<figure><img src="image_81.png" /><figcaption>**Figure 76** *Incolore* mutants in the *P. anserina* species complex. *Incolore* is due to dominant nuclear mutations conferring selective advantage to nuclei both during growth and stationary phase.</figcaption></figure>

in syncitia to the detriment of the wild-type nuclei and mycelia carrying them grow faster and produce abundant aerial hyphae. Hence, in laboratory conditions enabling nuclear division (i.e., when incubated at temperatures enabling cell division), *Incolore* nuclei accumulate in mycelia that are resting, even though the mutation rate of their appearance is low. Upon re-inoculation onto fresh media, nuclei carrying an *Incolore* mutation frequently and annoyingly take over the mycelium thanks to the faster growth of the *Incolore* mycelium. It is thus not recommended to store *P. anserina* and its sibling species at temperature above 4°C, if one does not want accumulation of *Incolore* mutations. *Incolore* nuclei, often mixed with wild-type ones, are found for example in most strains conserved in public collections (CBS, ATCC, DSMZ...). *Incolore* mutants are strongly counter-selected in nature since they are female sterile. Genetic analyses showed that *Incolore* mutations arise in several genes, none of which has been identified.

*Vauban* is another instability that manifests as highly frequent sectors (arrowheads) of abnormal growth. *Vauban* thalli end up looking like fortresses built by Vauban (1633-1707) as seen in figure 77.

<figure><img src="image_82.png" /><figcaption>**Figure 77** *Vauban*. Left, a typical thallus of *P. comata* strain T with numerous *Vauban* sectors at its edge. Middle, part of Neuf-Brisach fortress built by Vauban. Right, contamination experiments demonstrating that *Vauban* is due to the presence of a cytoplasmic and infectious factor.</figcaption></figure>
Although *Vauban* and Crippled Growth sectors look alike with more pigments, no aerial hyphae and female sterility and although they are likewise due to the presence of a cytoplasmic and infectious factors (figure 77), they are due to different molecular mechanisms. Indeed, *Vauban* sectors are not induced by stationary phase, they cannot be cured by applying stresses and they develop on M2 medium. *Vauban* has been detected in strains of *P. comata*, *P. pseudoanserina* and *P. pseudopauciseta*, but has not yet been observed in any strain of *P. anserina*. The mechanism generating *Vauban* is to date unknown, but similar sector phenomena are present in many filamentous ascomycetes and are suspected to be due to prions. Interestingly, *P. anserina* possesses a true prion that will be discussed in the next section. This prion does not cause any obvious morphological modification.

A last phenotypic instability called Wavy (figure 78) has been observed in mutants affected in potassium transporters of the TRK family. Unlike the above-described phenomena, the instability leads to several distinct phenotypes (at least three in addition to the “normal” one that looks like the phenotype of the wild type: “green and flat”, “green and zoned” and “white and zoned”). At the present time, it is unclear whether the various phenotypes result from a graded change in a single phenomenon, the mixing in various proportions of hyphae affected by a single bistable process or to several distinct phenomena. However, upon replica onto fresh medium, one usually observe a sequence of changes from “Normal”, to “green and flat”, then “green and zoned” and finally “white and zoned”. The switch is greatly influenced by the temperature (low temperatures promote the change towards the “white and zoned” phenotype, while high temperatures tend to promote the direction toward the “normal” phenotype). This suggests therefore that Wavy multistability is likely linked to changes in a single process. This is confirmed by the

<figure><img src="image_83.png" /><figcaption>**Figure 78** Wavy, a multi-stable phenotypic instability. Left and middle, the various phenotypes exhibited by the *PaTrk1*<sup>452</sup> mutant. Right, Right, contamination experiments demonstrating that *Wavy* is due to the presence of a cytoplasmic and infectious factor.</figcaption></figure>
fact that it is also created by a cytoplasmic and infectious factor (figure 78). There are two genes encoding such transporters in *P. anserina*, *Patrk1* and *PaTrk2*. The most important appears to be *PaTrk1*, because the phenotypic instability is more frequent in the mutants of this gene than in the one of *PaTrk2*. Paradoxically, mutants of *PaTrk1* impair Crippled Growth, as stated above. In these mutants, the Crippled Growth degeneration is thus replaced by the Wavy one!

Finally, as for other fungi, *P. anserina* mycelia exhibit phenotypic plasticity, i.e., their morphology is highly dependent upon growth conditions. For example, the origin of the water used to make the growth media has some influence on mycelium morphology and pigmentation, owing to the variable presence in trace amounts of various compounds such as calcium, manganese or even proteins produced by biofilms growing inside pipe tubes. This coupled with the above-discussed phenotypic instability makes it that mycelia on Petri plates from the same strain often look different with various shades of pigmentation, amounts of aerial hyphae, presence of more or less "waves" in the mycelium... Especially, mycelium features are affected by history. For example, longevity is dependent on the sizes of the explants used to inoculate mycelia onto fresh medium: the smaller the explants the shorter the longevity. Similarly, it is worth reminding that passage into stationary phase triggers Crippled Growth while stresses cure it... Nevertheless, *P. anserina* mycelia are easily recognizable and can be easily tamed, provided that few guidelines are followed for their handling. The most important ones are

- always replicate from the center of the thallus to avoid Senescence

- never store for a long time above 4°C to avoid *Incolore* mutation

- remember that if you replicate onto media enabling Crippled Growth, the degeneration will occur with nearly 100% frequency if the explants are taken in the center of the culture, which one does to avoid Senescence...

## Hyphal Interference and Vegetative/heterokaryon Incompatibility

Another field of intense research in *P. anserina* is the deciphering of molecular mechanisms of self versus non-self recognition. Indeed, G. Rizet discovered that *P. anserina* undergo a phenomenon now called vegetative, protoplasmic or heterokaryon incompatibility which involves recognition between *P. anserina* strains, as previously described for some other fungi (the phenomenon was first described in *Diaporthe perniciosa* in 1923 by D.M. Cayley). More recently, I pointed out that the friendly mold is also
<figure><img src="image_84.png" /><figcaption>**Figure 79** Hyphal Interference in *P. anserina*. Top, when *P. anserina* is confronted to other filamentous fungi, it produces at the meeting point high amounts of peroxide (black arrowheads), as visualized by the accumulation of the brown precipitate of diaminobenzidine. Similar processes called oxidative bursts are encountered in other instances of innate immunity in animals and plants, but also in other fungi such as *Coprinopsis cinerea* (arrows). Bottom, blue Evans/Trypan staining demonstrates that the contact may be associated with hyphal death (white arrowheads) or not as in the case of the confrontation of *P. anserina* with *Fusarium oxysporum*. *P. anserina* kills *Penicillium chrysogenum* and *Sordaria macrospora*. It is however killed by *C. cinerea*.</figcaption></figure>

able to defend itself against competitors by Hyphal Interference, a process previously discovered only in basidiomycetes by F.E. Ikediugwu & J. Webster in 1970, that involves the recognition of hyphae from other species of filamentous fungi. Hence, *P. anserina* is also able to recognize its hyphae from those of another species, but also differentiates between hyphae from vegetatively-compatible versus incompatible strains.

We shall briefly discuss first Hyphal Interference because much less is known on this process than on Vegetative Incompatibility. When *P. anserina* is confronted with other fungal species, it produces an oxidative burst (figure 79), a reaction commonly encountered during innate immunity reactions in animals and plants. The oxidative burst occurs specifically when *P. anserina* is confronted with hyphae of ascomycetes or basidiomycetes and not when confronted with inert materials such as glass or plastic, yeasts, bacteria or hyphae from *Mucoromycotina*. Hence, *P. anserina* is able to recognize that it encounters another *Dikarya* filamentous fungus. Importantly, when confronted with another *P. anserina*
<figure><img src="image_85.png" /></figure>

**Figure 80** Lack of Hyphal Interference between strains of *P. anserina* and presence of hyphal interference between *P. anserina* and *P. pauciseta*. *Podospora pauciseta* CBS 237.71 and the BIG S and small s strains of *P. anserina* were inoculated along diverging lines as indicated on the left scheme. After three days, the DAB staining shows a lack of oxidative burst when the BIG S and small s strains of *P. anserina* are confronted; yet cell death due to vegetative incompatibility (light blue arrow) occurs at the confrontation between the two vegetatively-incompatible strains of *P. anserina* as shown by the Evans Blue staining. On the contrary, an intense oxidative burst on both *P. anserina* and *P. pauciseta* mycelia (red arrows) occurs at the junction between *P. anserina* and *P. pauciseta*, along with many hyphal death (dark blue arrow).

strain, such as in the confrontation between the vegetatively-incompatible BIG S and small s strains, no oxidative burst happen (figure 80), showing that the fungus can differentiate between self and non-self at the species level. This recognition does not necessitate the fusion of hyphae, but requires nonetheless a contact between the hyphae of the two contestants. Although the burst is a constant feature during the interactions between *P. anserina* and another species, the outcome is variable. Indeed, confrontation may or may not be accompanied by the death of the contestant or that of *P. anserina* (figure 79). Interestingly, an oxidative burst often associated with cell death occurs at confrontations between strains of the different species of the *P. anserina* species complex (figure 80 and 81), further confirming that these are bona fide species.

Analyses of mutants have shown that the burst and death during confrontation with *Penicillium chrysogenum*, the main fungus used in Hyphal Interference test, is under the control of the PaMpk1 MAP kinase pathway and in part the PaNox1 NADPH oxidase complex, but does not require the PaMpk2 and PaMpk3 MAP kinase pathways or the PaNox2 and PaNox3 NADPH oxidase complexes. Intriguingly, some of these complexes and pathways control Crippled Growth (see previous section); yet, the connections
<figure><img src="image_86.png" /><figcaption>**Figure 81** Hyphal Interference between strains of *P. anserina* species complex. Species of the complex show variable amount of oxidative burst and cell death when confronted with each other.</figcaption></figure>

between the two phenomena are unclear. However, Hyphal Interference against *Penicillium chrysogenum* is efficient in *P. anserina*, which present Crippled Growth, and inefficient or even absent in other species of the *P. anserina* species complex that do not present Crippled Growth. Mutant analyses have also shown that the oxidative burst and hyphal death are not correlated, for example a mutant affected in the TIM54 protein controlling the import in the mitochondria has a large increase of the oxidative burst and a much decreased hyphal death. At the present time, little more is known about this fascinating process.

Unlike Hyphal Interference, Vegetative Incompatibility requires the fusion by anastomosis of hyphae to take place. This phenomenon occurs thus when two genetically-different strains of *P. anserina* meet (figure 82). The phenotypic features of the incompatibility reaction include morphological modifications of the vacuoles from tubular to round, increased septation, accumulation of lipid droplets, abnormal deposition of cell wall, reduction in cytosolic protein translation and activation of phenoloxidases, dehydrogenases and proteases. This culminates with the cell death of the hyphae containing the genetically-incompatible nuclei (hence the alternative name of Heterokaryons Incompatibility), likely due to the ruptures of the membranes of the vacuoles and the whole cell. Interestingly, a role of autophagy in delaying cell death has been evidenced.

The genetic differences that trigger the incompatibility reaction are located in specific genes, called *het* genes (for *heterokaryons incompatibility genes*). Nine het genes have been identified so far in *P. anserina* (figure 83). Two kinds of incompatibilities are known: allelic incompatibilities in which presence of different alleles of the same gene inside the same cytoplasm triggers the death reaction and
<figure><img src="image_87.png" /><figcaption>**Figure 82** Vegetative incompatibility between the S and s strains. Left, compatible (white arrow) and incompatible (black arrow) confrontations between the progeny of a S x s cross and a S tester. Right, microscopic visualization of the incompatibility reaction: (A) hyphae after anastomosis formation and (B) a few minutes later when the incompatibility reaction has occurred. Photos courtesy B. Turcq.</figcaption></figure>

non-allelic incompatibilities in which specific combinations of alleles of different genes inside the same cytoplasm cause the incompatibility reaction (figure 83). The multiplicity of *het* genes, along with the multiplicity of alleles in non-allelic incompatibility (figure 83), results in a large number of different compatibility group and warrants that in the wild, most encounter between *P. anserina* strains are incompatible.

The identification of *het* genes has led to very interesting insights into the mechanisms of allorecognition in fungi, as well as to the identification of a prion protein; indeed, Rizet showed in the early fifties that the *het-s* allele involved in the allelic *het-S/het-s* vegetative incompatibility exhibits a peculiar behavior that is now explained by the ability of the het-s protein to self-catalyze a fold change into amyloid aggregates, a hallmark of prion. It is beyond the content of this book to retrace the whole history of the discovery of the het-s prion and I refer to the numerous reviews on the subject, suffice to say that the prion was first discovered genetically by G. Rizet thanks to the weird changing properties of the het-s allele in incompatibility reaction (figure 84). Identification of the *het-s* and het-S genes and subsequent analyses demonstrated clearly that het-s was a prion, while het-S was not (figure 84). It was the first cellular prion for which infectivity was clearly linked to aggregation by transforming recipient prion-free strains with amyloids and for which a structure of the aggregated form was obtained (figure85). Importantly, the het-s amyloids are not toxic to the fungus *per se*, but must interact with an
<figure><img src="image_88.png" /><figcaption>**Figure 33** Genetic control of Vegetative Incompatibility in *P. anserina*. Top, nine identified loci involved in the control of Vegetative Incompatibility. Bottom, ♂ identifies lethal combinations of het-c/het-d and het-c/het-e alleles.</figcaption></figure>

additional partner to trigger death. This partner can be the het-S protein. Upon binding of the het-S protein to the het-s amyloid, a Helo domain of het-S is unmasked. This Helo domain interacts with the cell membranes that it disrupts. It is most likely that cell death results for leakage of the cellular content. In this system, recognition between self and non-self is thus effected by the prion-like aggregation of het-S templated by the het-s prion.

Interestingly, it has been observed that a gene encoding a NOD-like receptor called *nwd2* lies beside *het-S*, while it is present as a pseudogene beside *het-s* (figure 84). NOD-like receptors bind ligands, especially, pathogen-associated-molecular-pattern or pamp that are accompanying pathogens, resulting in a conformational change of the receptor and transmission of a signal to counteract the pathogens. Pamp recognition is accomplished by a WD domain, carrying WD40 repeats. The genome of *P. anserina* S strain contains 77 of such genes. Interestingly, the *het-d*, *het-e*, *het-r* and *het-z* genes also encode NOD-
<figure><img src="image_89.png" /></figure>

**Figure 84** The het-s prion. Left, Rizet observed that strains carrying the het-s allele can adopt two mutually exclusive phenotypes: the het-s one in which the cultures are incompatible with strains carrying het-S and the het-s* one, in which the cultures are compatible (top left). Rizet observed that het-s* cultures convert spontaneously at low frequency towards het-s and that this can be triggered with 100% efficiency when het-s* is in contact with het-s and anastomoses occur (middle left): het-s is thus infectious to the detriment of het-s*, so that eventually all cultures carrying het-s end up being het-s. Het-s* cultures can nonetheless be recovered after sexual reproduction since progeny carrying the het-s allele are het-s* (bottom left); note that if the female parent is het-s, some progeny is directly het-s. All the properties of the het-s allele and its interactions with the het-S one are now explained by the prion properties of het-s (right). Upon translation of its messenger, the C-terminus of the het-s protein, which is the prion-forming domain, is unfolded and the het-s protein does not interact with het-S: the strain is thus het-s*. Folding of the het-s prion-forming domain into an amyloid structure is spontaneous at low frequency and results in more het-s monomers joining the amyloid fibers, explaining the spontaneous conversion of the het-s* phenotype into het-s and the infectiosity of het-s. Importantly, the het-S protein is also able to join the het-s amyloids, although it cannot form alone amyloid. Upon joining the amyloid a Helo domain carried by het-S is unmasked (this Helo domain is not present in het-s). The unmasked Helo domain disrupts membranes triggering cell death, which occurs thus only in the presence of both the het-s amyloids and het-S. It has been demonstrated that the ndw2 protein, whose gene is located beside het-S (this gene is present as a pseudogene beside het-s) can also template amyloid formation. It is speculated that it is triggered to do so by an as-yet unknown effector and that the formed complexes with het-s and/or het-S may be involved in pathogen recognition and elimination.
<figure><img src="image_90.png" /><figcaption>**Figure 85** Structure of the het-s prion-forming domain. The prion-forming domain of het-s is located at the C-terminus of the protein. Here, several monomers are folded into an amyloid fiber.</figcaption></figure>

like receptors and a model has been proposed and demonstrated to account for their role in vegetative incompatibility. In the case of nwd2, it has been demonstrated that chimaeric NWD2 proteins carrying WD-domain with known activating effectors is able to seed the formation of the het-s prion when they are activated by the cognate ligand, showing that the amyloid fold can be transmitted to het-s by an activated NOD-like receptor. The actual activating effector of the NWD2 protein is unknown, but is speculated that it is a pamp and that upon activation by the effector the fold is transmitted to the het-S or het-s proteins and that this participate in the pathogen detection and/or elimination (figure 84).

In the case of het-d and het-e, the fold change is transmitted to the het-c protein. Cloning identified *het-c* as a gene encoding a glycolipid transfer protein able to transfer glycolipids between vesicles *in vitro*, but whose cellular role in still unknown. Inactivation of *het-c* led to a defect in the production of normal ascospores, indicating an important role during their maturation. Presently, 11 different alleles of this gene have been identified in natural populations. They define seven specificity groups of incompatibility with *het-d/het-e* alleles (figure 83). Like for the het-s/het-S complexes, the incompatible het-c/het-d or het-c/het-e complexes interact with the plasma membrane, resulting in its disruption. In the case of het-z, the protein interacting with the het-z1/het-z2 complex and effecting death is PaSec9, an essential SNARE protein involved in vesicle fusion, suggesting that membrane disruption is also involved in hyphal death in this incompatibility system. At the time of writing this book, the het-r protein has not been investigated thoroughly and the *het-v*, *het-B* and *het-Q* genes have not been identified.

The involvement of NOD-like receptor suggests that in nature the components involved in Vegetative Incompatibility not only act to monitor self *versus* non-self recognition in *P. anserina*, but also as a defense system against pathogens, especially bacteria. This hypothesis is further supported by the fact that the transcriptional responses to the presence of bacteria and the one during an incompatible
reaction overlap. During Vegetative Incompatibility, the system would act to limit the spreading of potential deleterious elements present in the cytoplasm, especially virus-like particle as shown in *Cryphonectria parasitica* (there is presently no true viruses having an extracellular phase described in fungi, but genetic elements having all hallmarks of viruses are widespread in these organisms), or mitochondrial plasmids that may alter lifespan. It has also been postulated that the death system active during Vegetative Incompatibility could be activated to provide nutrients during stationary phase and especially during sexual reproduction in the hyphae underlying maturing fruiting bodies. Indeed, many mutants having suppressed Vegetative Incompatibility are female sterile, have increased amounts of aerial hyphae and impairment in growth renewal after exit of stationary phase. Moreover, Vegetative incompatibility between strains is often associated with sexual incompatibility, *i.e.*, in many instances, crosses between vegetatively-incompatible strains are partially or totally sterile and these sterilities are controlled by the *het* genes. Whatever the actual roles of this executed hyphal death, the polymorphism of the genes involved in Vegetative Incompatibility is under balanced selection, suggesting an active evolutionary force to maintain the polymorphisms of the *het* genes, a feature compatible with a role in pathogen defense and self *versus* non-self recognition. This is clearly exemplified by the het-z/sec9 incompatibility system, since it is conserved in *Neurospora crassa*, but also in the distantly related *C. parasitica*.

## Appressorium-like structure differentiation

The full extent of cellular differentiation during vegetative growth that *P. anserina* is able to achieve is unknown. We know that it is able to produce small apical hyphae and that in stationary phase larger hyphae are produced, especially those that underlie the maturing fruiting bodies. *P. anserina* is also able to produce aerial hyphae in about 24 hours, most likely coated with hydrophobins and it is very efficient to produce anastomoses as early as 4 hours after growth (see chapter on morphology and cytology of the mycelium; figure 86). Nevertheless, the most striking hyphal differentiations that *P. anserina* is able to produce are the appressorium-like structures, penetration pegs and haustorium-like structures involved in plant biomass penetration (see chapter on morphology and cytology of the mycelium; figure 86). These are easy to visualize when the fungus is grown on cellophane overlaying a medium devoid of glucose (such as M2 and M0, see figure 37) and differentiate in 12-24 hours. Note that
<figure><img src="image_91.png" /><figcaption>**Figure 86** Differentiation during the vegetative phase of *P. anserina*. See figures 33, 35 and 37 for actual pictures.</figcaption></figure>

if we don't know the molecular pathways implicated in the erection of hyphae, anastomosis is under the control of the IDC genes involved in the making of the C element associated with Crippled Growth (see section on Crippled Growth). For penetration of cellophane, it was shown that reorientation of hyphae towards cellophane and formation of the appressorium-like structures are under the control of the same molecular pathway as the one controlling ascospore germination, i.e., the PaNox2/PaPls1 NADPH oxidase complex and the PaMpk2 MAP kinase (see section on ascospore ejection and germination). Later stages of the differentiation are less well known; however, the formation of the penetration peg is under the control of the PaNox1/PaNoxD NADPH oxidase.
## Sexual reproduction

Sexual reproduction of *P. anserina* has been under scrutiny for a long time. Indeed, the first studies using *P. anserina* as an experimental system, i.e., those of Wolf in 1912 and Satina in 1916, were on sexual development. Since then, numerous studies have been published; including some dealing with the recognition between the sexual partners, i.e., the mating system of *P. anserina*, the differentiation of its fruiting bodies and their production and repartition on the mycelium. Additional mechanisms acting during sexual reproduction have also been studied, including Spore Killers and RIP.

## Mating and mating types

As explained in the section dealing with the life cycle of *P. anserina*, the fungus is pseudo-homothallic, implying that fertilization can only proceed between sexually-compatible partners: one *mat+* and one *mat-*. Genetic analyses have indicated, that half the nuclei obtained after meiosis are *mat+* while the other half is *mat-*; the mating system of *P. anserina* is thus akin to the bipolar heterothallism found in many ascomycetes. Hence, there is a single sexual locus with two alternative versions, one conferring the *mat+* identity and the other the *mat-* one. As the mating type was the first genetic marker available for *P. anserina*, this *mat* locus, which branded genetically a first chromosome, was positioned on chromosome 1.

Identification of the two *mat* loci was achieved with the help of the cloned *matA* locus of *Neurospora crassa*, by heterologous hybridization of a genomic bank. We now know that the *mat+* idiomorph contains one gene, *FPR1*, while the *mat-* idiomorph contains three genes, *FMR1*, *SMR1* and *SMR2* (idiomorphs are alternative versions of a locus that contain different genes rather than different alleles of the same gene(s); figure 87). *FPR1* and *FMR1* are the two genes important for the recognition between the partners, e.g., for fertilization, while *SMR1* and *SMR2* are important for ensuing ascospore formation. As stated in the section on "Developmental genetics: grafting and genetic mosaics", the
<figure><img src="image_92.png" /></figure>

**Figure 87** Structure and regulation of the mating type loci of *P. anserina*. Top, like in most ascomycetes the mating type loci of *P. anserina* are bordered by the *APN2* and *END4* genes. The region different between the *mat+* and *mat-* strains are boxed in pink and the mating type genes are in red. Bottom, the network of HMG-box transcription factors involved in regulating the expression of the *FMR1* and *FPR1* mating type genes, which in turn activates the PRE1/MFM and PRE2/MFP receptor pheromones genes, respectively. The thickness of the arrows is proportional to the strength of the activation (arrow) and repression (blunted line)

deletion of the mating type result in a strain (Δ*mat*) completely unable to engage fertilization with either a *mat+* or a *mat-* partner. However, Δ*mat* differentiate normally spermatia and ascogonia. It also produces protoperithecia. This underscores that the mating type solely controls the formation of the
<figure><img src="image_93.png" /><figcaption>**Figure 88** Structure of the mating type locus of the *mat+*_ *mat-* dual mater strain PM154</figcaption></figure>

zygotic tissue of the fruiting body, but not that of the gametes and the first stages of the maturation of the ascogonia into protoperithecia. Through *SMR1* and *SMR2*, but also *FPR1* and *FMR1*, the mating type locus also controls later stages of ascospore production, especially the nuclear recognition that must take place for the production of the dikaryotic *mat+/mat-* ascogenous hyphae that will lead to ascus genesis. *Δmat* can also be used to help the development of mutant affected in the maternal tissue of the fruiting body (see section on "Developmental genetics: grafting and genetic mosaics"), indicating that the mating-type locus is not involved in the differentiation of the maternal tissues of the fruiting bodies, but solely the zygotic one. Alternatively, there is a mutant of *P. anserina*, called *vacua*, in which normal looking perithecia are developing in the absence of fertilization. These contain only paraphyses and are devoid of asci, confirming that it is possible to uncouple the development of the zygotic tissues resulting from fertilization from that of the maternal tissue, *i.e.*, the peridium and other non-zygotic tissue of the centrum.

Introduction of a *mat+* idiomorph into a *mat-* strain results in a mutant able to mate with both *mat+* and *mat-* strains, but also able to self-fertilize. A *mat+_mat-* dual mating strain was even created by introducing cleanly (*i.e.*, without additional sequences) the *mat+* idiomorph beside the *mat-* one at the mat locus of chromosome 1: the *PM154* strain (figure 88; see section on "Developmental genetics: grafting and genetic mosaics" for the use of this strain in mutant search).
<figure><img src="image_94.png" /><figcaption>**Figure 89** Roles of *P. anserina* pheromones and receptors in mating. Targeted deletions have shown that mutants lacking *MFM* or *MFP* are male sterile in a mating-type specific manner: *mat+* spermatia lacking *MFM* are unable to engage fertilization while *mat+* spermatia lacking *MFP* are fully functional; the converse is true for *mat-* spermatia. Similarly, mutants lacking *PRE1* or *PRE2* are female sterile in a mating-type specific manner: *mat-* ascogonia lacking *PRE1* are unable to engage fertilization while *mat-* ascogonia lacking *PRE2* are fully functional; the converse is true for *mat+* ascogonia. Therefore, *mat+* spermatia attract the *mat-* trichogynes expressing *PRE1* through the production of the MFM pheromone and the *mat-* spermatia attract the *mat+* trichogynes expressing *PRE2* through the production of the MFP pheromone.</figcaption></figure>

In *P. anserina*, gametes are present on mycelia older than three days. Accordingly, expression of *FMR1* and *FPR1* is significant only after three days. It was shown that expression of both genes is under the complex control of a set of transcription factors containing HMG-box as DNA-binding domain (figure 87). Note that three out of the four genes present at the mating type locus (*FPR1*, *FMR1* and *SMR2*) also encode transcription factors containing HMG-box, while the last one (*SMR1*) has no obvious associated function or known domain and is not actually involved in defining sexual identity (this gene is necessary for ascospore production but can act in the *mat+* and *mat-* nuclei or in both, it appears involved at later stages of the fruiting body development than *FPR1*, *FMR1* and *SMR2*). Overall, 11 out of 12 HMG-box-containing proteins encoded in the *P. anserina* genome are involved in the sexual cycle, many of which participate in conferring sexual identity. Intriguingly, a similar function has been attributed to HMG-transcription factors in mammals!

The whole sets of targets of *FMR1* and *FPR1* were identified through microarray analyses. Functional analyses of these targets identified few genes actually involved in sexual development apart from the receptors *PRE1*/*PRE2* and the previously characterized mating pheromones *MFP*/*MFM* (figure 87). Functional analyses have shown that, as expected, spermatia produce sex-specific pheromones that
attract the trichogyne of opposite mating type and expressing the cognate receptor (figure 89). The fact
that many genes regulated by *FPR1* and *FMR1* are not involved in sexual reproduction suggests that both
mating-type transcription factors are involved in the control of other processes in *P. anserina*.

Finally, it worth mentioning that the mating type locus is embedded in a 800 kb-region devoid of
recombination, so that numerous polymorphisms exist between the *S mat+* and *S mat*- strains in this
region, while their sequences is strictly identical in the rest of the genome. Additionally, many genes are
differentially regulated between the *mat+* and *mat*- strains independently of the mating-type locus, *i.e.*,
thanks to differences present in the non-recombining region. In some *Neurospora tetrasperma* strains,
another pseudo-homothallic fungus, lack of recombination is linked to the presence of inversions in the
genome. In *P. anserina*, the mechanisms preventing recombination is still mysterious as no inversion have
been detected around the mating type locus. As explained in the chapter on "the sexual cycle and
genetical analysis", *mat+/mat-* dikaryotic ascospores are obtained through a defined arrangement of
nuclei in the postmeotic mitosis coupled with the fact that in most meiosis (in ~99% of them) a single
crossing-over occurs between the centromere of chromosome 1 and the mating-type locus. Possibly, the
same mechanism that regulates the positive interference inhibiting the occurrence of a second crossing-
over between the centromere and the *mat* locus also intervene to inhibit the recombination around the
mating type. Whatever the mechanism, the differences observed in the non-recombining region are not
involved in the maintenance of the heterokaryosis necessary for self-fertilization through fitness-
enhancing complementation. Indeed, heterokaryons are very stable in *P. anserina*, whatever their genetic
constitution at the mating-type locus.

Fruiting body differentiation

Fruiting body differentiation is also intensively studied in *P. anserina*. As explained in the
perithecium section on "Morphology and cytology" chapter and the section on "Developmental genetics:
grafting and genetic mosaics" of the chapter on "The sexual cycle and genetical analysis", the fruiting
body is made up of zygotic tissues (the lineage leading to asci) resulting from fertilization and maternal
ones that originate from hyphae neighboring the fertilized ascogonium (figure 90). The mycelium is also
an important partner acting in the feeding of the perithecia and dedicated large hyphae connect
maturing fruiting bodies to the underlying mycelial network (figure 90). Respective roles of genes in these
<figure><img src="image_95.png" /><figcaption>**Figure 90** The three components interacting to produce mature fruiting bodies. In red, the zygotic tissues, in blue the maternal tissues and in green the mycelium.</figcaption></figure>

three interacting components involved in the elaboration of the fruiting body can be analyzed thanks to genetic analyses adapted from embryology technics developed in animals, e.g., genetic mosaics and grafting (see “Developmental genetics: grafting and genetic mosaics” section of the chapter on “The sexual cycle and genetical analysis”).

The zygotic lineage develops only after fertilization. Fertilization leads first to the production of a plurinucleated cell containing both *mat+* and *mat*- nuclei. From this plurinucleated cell, ascogenous hyphae emerge. These carry a single *mat+* nucleus and a single *mat*- one. How, nuclei of opposite mating types recognize each other is unknown. Based on the phenotypes of *FPR1*, *FMR1* and *SMR2* mutants it has been proposed that the three mating type genes also participate in the recognition between the sexual partners at this stage (mutants of these genes produce selfish nuclei that engage ascus development in the absence of a mating partner and hence undergo haploid meiosis). Note that at this
stage, recognition occurs between nuclei. Accordingly, recognition does not require the mating pheromones and their receptors. Once two nuclei have properly recognized each other, *SMR1* would be required to lift a process that blocks further development of the zygotic lineage. Indeed, the *SMR1* gene of the *mat*- mating type is required for the production of the ascogenous hyphae. The PaRID DNA methyl transferase is also required at this stage. DNA methyltransferases are involved in defining DNA methylation patterns. In *P. anserina* as in other *Pezizomycotina*, RID DNA methyltransferases are also involved in the Repeat-Induced Point mutation process or RIP, a feature that will be discussed in a previous section (see the “RIP” paragraph in the section on “Genes and genome” in the chapter on “The sexual cycle and genetical analysis”). How PaRID control development is unknown, especially since no DNA methylation has been observed yet in *P. anserina*, and since, unexpectedly, the methyltransferase catalytic domain is important for the function of PaRID during development. However, transcriptome analyses have shown that genes regulated by PaRID overlap those regulated by the mating type. Note that, alternatively to *mat+* and *mat-*, the two nuclei engaging recognition can be viewed as paternal and maternal ones. Owing to the different ontogeny of spermatia and ascogonia, it is possible that their nuclei are branded with different epigenetic marks (imposed by PaRID?), which could facilitate the recognition between the two nuclei (and a feature that would also explain the lack of germination of spermatia).

Nothing is known about the coordinate divisions of the ascogenous hyphae preceding the production of croziers. More is known about the genesis of croziers. They require the *cro1* and *ami1* genes since mutants of these genes have abnormal croziers, plurinucleated ones for *cro1* mutants and uninucleated ones for *ami1* mutants. The *cro1* protein shares some similarity with UCS proteins that are involved in folding, assembly and function of myosin, while *ami1* is similar to *Aspergillus nidulans* apsA, a cortical protein that controls spindle positioning during mitosis. Both mutants have additional defects, indicating supplementary roles. The *ami1* mutants have abnormal nuclear positioning in mycelia and asci and produce anucleated spermatia and periphyses. The *cro1* mutants display normal septation and nuclear positioning, but have abnormal mycelium morphology and a germination defect. The next step of sexual development, i.e., the commitment of croziers into meiocytes (ascus) in which caryogamy proceeds necessitates some as yet undefined peroxisomal protein(s) as many of the proteins involved in peroxisomal import accumulate croziers that do not engage into further development (figure 91).
<figure><img src="image_96.png" /><figcaption>**Figure 91** Peroxisomes and ascus development. Left, phenotype of the wild type and of peroxisome mutants, in which croziers accumulate without engaging into ascus development. Right, the subunits of the peroxisome import machinery labelled in purple are required for commitment into meiocytes, those in blue are not. The actual peroxisomal protein(s)/product(s) required for the transition are(is) unknown).</figcaption></figure>

The next stage of sexual development is meiosis. *P. anserina* is not as used as *Sordaria macrospora* for meiosis analyses owing to the small size of its nuclei during this stage. Nevertheless several mutants affected in meiosis are available. Two have been studied. Firstly, mutants of the mitochondrial citrate synthase, the initial enzyme of the Krebs respiratory cycle are blocked at the diffuse stage of the first meiotic prophase, identifying a metabolic checkpoint for meiosis progression beyond this point. Secondly, the PaMe4 encoded by the *mei4* gene is a component of the synaptonemal complex and spindle pole body having crucial roles in their morphogenesis and later in recombination complex formation. Intriguingly, the Meiotic Silencing by Unpaired DNA (MSUD) process present in some *Neurospora* spp. appears absent in *P. anserina* since unpaired essential genes, such as the *AS4* gene encoding the cytosolic elongation factor, can pass through meiosis without problem. MSUD silences DNA regions that are not paired during prophase of the first meiosis through an RNA interference mechanism. Nevertheless, the expected fluorescence of proteins tagged with the GFP or mCherry proteins is often absent in the young sexual tissues for an unknown reason. Note that we also have no convincing evidence for the occurrence in *P. anserina* of Quelling, a second RNA interference mechanism acting during the vegetative phase in *Neurospora crassa*, although we sometime observe extinction of transgenes expressing proteins tagged with GFP or mCherry in the mycelium.

Several mutants having defects in later stages of development, i.e., ascospore formation and
expulsion are available. It is however not known whether these have specific alterations in the ascospore
formation developmental program have general disturbance in metabolism, which being higher during
ascospore formation could result in various impairments. For example, many peroxisomal mutants have
abnormally-pigmented ascospores that germinate at lower frequency. Fidelity of the cytosolic translation
has also been shown to have a major impact on fertility. Mutants with lower fidelity are female-sterile,
while some with higher translation accuracy have ascospore formation defects and others are female
sterile. It has been shown that the ascospore formation defect is linked to increased accuracy, suggesting
that mistranslation of some key regulator(s) is required for proper development of ascospores. Also,
some mutants of potassium transporters do not properly expel their ascospores unless the medium is
supplemented with large amounts of potassium, while others have the opposite phenotype, depending
on whether they are involved in taking in potassium or expelling excess of it. One more mutant is worth
of mention: the one affected in the *PaAlr1* gene, encoding a magnesium transporter. Null mutant of this
gene has the development of all its ascospores arrested at the stage when they contain two nuclei.
Reason for such a distinct defect is unknown.

As seen from the above text, our knowledge of zygotic tissues development in *P. anserina* is still
very patchy. One of the reasons for this fact is that few mutants affected in the zygotic lineage are
available. Indeed, for a long time, it was difficult to isolate recessive mutations with zygotic defect since
*P. anserina* being formally heterothallic; mutations need hence to be present in both parents to exert
their effect (note that mutants affecting maternal tissues were easily obtained since they were female-
sterile!). Screening for recessive mutants required thus time-intensive genetic manipulation on many
candidates to obtain few interesting mutants. Thanks to the availability of the *mat+*_ *mat*- self-fertile
strain PM154 screening of recessive mutants is now very easy (see "Developmental genetics: grafting and
genetic mosaics" section of the chapter on "The sexual cycle and genetical analysis"). So far a single
mutant obtained thanks to this strain has been thoroughly analyzed; it has both zygotic and maternal
defects: *spod1*. The zygotic defect in *spod1* occurs after the first prophase of meiosis. Older asci are
enlarged; they contain many nuclei and later on undergo lysis. The *spod1* mutant has also a strong
maternal defect and produce tiny abortive fruiting body. The gene affected in *spod1* encodes an inositol-
phosphate polykinase, a protein involved in signaling through phosphorylation of inositol-phosphate
molecules in eukaryotes. We shall again return to this mutant in the next section because it has
interesting phenotypes pertaining to the localization of fruiting bodies on the mycelium. But before we
do so, we must discuss the signaling pathways involved in the development of the maternal tissues.
Indeed, in addition of *spod1*, many mutants affected in maternal tissues development have been
analyzed in *P. anserina*.

<figure><img src="image_97.png" /><figcaption>**Figure 92** Model of action of the roles of IDC genes during peritheium maturation. From top left to bottom right. Development starts with fertilization. This triggers the release of an unknown signal from the zygotic tissues towards the maternal ones. In the maternal tissues, the PaNox1 NADPH oxidase complex is activated and starts to produce reactive oxygen species (ROS). The PaPsr1, PaWhi2, PaSo, IDC1 and PaPro1 proteins are also required in the maternal tissues for proper development. The ROS signal is likely transmitted through the voyage of vesicles containing oxidized IDC2 and IDC3 proteins; these proteins contains evolutionary-conserved cysteines required for their activity and genetic mosaics indicated that they act in a cell-non-autonomous manner (hence diffuse from cells to cells). Once in the underlying mycelium, they transmit their signal to the PaMpk1 and PaMpk2 MAP kinases pathways (in a manner that do not require thioredoxins). Once activated MAP kinases likely orchestrate the mobilization of the nutrients required for proper maturation of perithecia. The IDC1, IDC4 and PaPro1 proteins are also required in the mycelium. Not depicted here is the STRIPAK complex that is also important for peritheium production, it is required in the zygotic tissues but at a late stage of ascospore production, in the maternal tissues and in the underlying mycelium.</figcaption></figure>
<figure><img src="image_98.png" /><figcaption>**Figure 93** Lack of neck in mutants affected in homeodomain transcription factors. *Pah5* has the strongest effect since all perithecia produced by null mutants of *Pah5* lack neck, while null mutants affected in *Pah2* produce 30% of neckless perithecia. Other *Pah* genes have modulatory effect on the percentage of neckless perithecia produced by *Pah2* mutants. For example, a double mutant affected in both *Pah1* and *Pah2* produce 95% of neckless perithecia.</figcaption></figure>

First and foremost are the *IDC* mutants involved in Crippled Growth. Indeed, as stated in the section on "Crippled Growth and other phenotypic instabilities", mutants involved in making up *C*, the infectious element associated with Crippled Growth, lack development of fruiting bodies after fertilization, while they produce male and female gametes. Only one of these mutants, the one affected in the PaPro1 transcription factor is affected in the formation of the zygotic tissues, all the other are dispensable for proper development of the zygotic tissues and hence their fertility defect is due to impairment in the production of the maternal tissues. How PaPro1 is involved in the formation of the zygotic tissues is unknown, but its action takes place very early during the process and may even occur at the fertilization stage. For the other *IDC* mutants, analyses using genetic mosaics and grafting has enabled to determine which component(s), *i.e.*, the mycelium or the maternal tissues, is(are) important for the maturation of the fruiting bodies, leading to the model depicted in figure 92. The major feature of this model is that fruiting body development results from the Reactive Oxygen Species (ROS) emitted by the maturing fruiting bodies thanks to the activation of the PaNox1 NADPH oxidase complex to the underlying mycelium through vesicular transport of the oxidized IDC2 and IDC3 proteins. There, they activate the PaMpk1 and PaMpk2 MAP kinases, which participate in nutrient mobilization to feed the maturing perithecia. Accordingly, microarray analyses of transcriptomes have shown that PaMpk1 and
PaMpk2 regulate genes involved in carbohydrate metabolism.

Transcription factors have also been analyzed for their involvement in the development of the maternal tissues of the fruiting bodies. The HMG transcription factors Pahmg6, Pahmg8 and kef1 are required in them for maturation of perithecia, while Pahmg1 is required in both the maternal and zygotic tissues. Transcription factors containing homeodomain have also been investigated and some were shown to be specifically involved in neck differentiation. The Pah2 and especially Pah5 transcription factors are important for this task since mutants have neck defects (figure 93). Note that the neck is a major morphological attribute and an important feature of the fruiting body enabling correct expulsion of ascospores. Most species related to *P. anserina* produced perithecia with neck, but a few ones produced neckless perithecia, that are then coined cleithothecia or more properly cleistothecoid perithecia.

In conclusion, *P. anserina* is invaluable in deciphering the development of the fruiting body. The pathways identified in the friendly mold have been shown to participate in development in other fungi, especially in its cousins *Neurospora crassa* and *Sordaria macrospora*, indicating as expected a conservation of these pathways in related fungi. However, there is still a lot of work to be done since, like in the other studied fungi, our understanding of its development is incomplete. The friendly mold is invaluable since the genetic tools used to differentiate the place(s) of action of the various actors (e.g., the genetic mosaics and grafts) are to date implemented only in this species.

## Fruiting body production and repartition

As stated in the chapter on "Mycelium growth and development", *P. anserina* is rather fussy when it comes to produce perithecia, at least more than during its vegetative phase. In addition, there are likely complex interactions between the factors regulating sexual development, because factors found to be absolutely required for perithecium production by some researchers, are found dispensable by others. For example, James E. Pehram in his thesis states that biotin can be omitted from the medium for optimal fertility, while we find it mandatory to obtain perithecia. Caution must thus be taken when interpreting the factors described below. Firstly, as stated in the chapter on "Mycelium growth and development, "*P. anserina* requires a medium not too rich in easily digestible carbon and nitrogen sources (such as glucose and ammonium). On rich medium, *P. anserina* produces large amount of mycelium, especially aerial hyphae, but remain sterile or produces usually with a delay abnormal
<figure><img src="image_99.png" /></figure>

**Figure 94** Effect of light on peritheium development in *P. anserina*. Left, M2 Petri plates were inoculated with *mat+/mat-* heterokaryotic inocula and incubated for eight days with or without light. The illuminated plate has more perithecia that have already started to expel ascospores, while the non-illuminated one has much fewer perithecia that are not yet mature. Right, M2 Petri plates were inoculated with *mat+/mat-* heterokaryotic inocula and incubated for eight days in constant illumination coming from above either with the lid on top or with the lid on the bottom, hence with plates upside down. On the plate with lid on the top, necks have an upright position pointing towards light, while on the plate with the lid on the bottom, necks tends to curve towards the medium, hence trying to also point towards the direction the light is coming from. Note that in both instances, necks are differentiated from the middle of the part of the perithecia that is sticking into air, and not within the medium for upside down plates.

perithecia producing few asci. Secondly, as stated above, in addition to thiamin, it requires biotin for optimal peritheium production, hence the presence of both vitamins in the minimal M2 medium. Thirdly, it requires light. Indeed, continuous light speeds up maturation and increases greatly maturation (figure 94). Light also directs the orientation of necks and hence the path of ascospore ejection (figure 94). Fourthly, efficient peritheium production requires air. On M2, perithecia are produce at the interface between the medium and the air. In M2 liquid cultures, *P. anserina* produces abortive perithecia, except for those few that are fortunate to develop at the interface between liquid and air. The likeliest explanation is that high levels of oxygen are required for the "Reactive Oxygen Species" production that controls peritheium production (see previous section). In other medium, such as M4, perithecia may be produced within the agar, always more slowly than at the air/medium interface. Their necks tend then to be produced arbitrarily on the top part of the fruiting body ("horizontal" perithecia are frequent when they develop inside the medium). This suggests a negative geotropism of the determinants that determine the position where they are differentiated. Finally, temperature is also important, since perithecia are efficiently produced between 18°C and 27°C. At lower temperature, the slow growth speed and very slow timing of peritheium production makes it difficult to obtain them. At 18°C on M2, perithecia take about three weeks after mycelium inoculation to mature, at 23°C they take
<figure><img src="image_100.png" /><figcaption>**Figure 95** Non-random repartition of fruiting bodies on *P. anserina* thallus. Left: typical repartition of fruiting body along a ring when *P. anserina* is cultivated on M2 at 27°C with constant illumination. Right, a fairy ring differentiated by basidiomycetes.</figcaption></figure>

about 9-10 days, and at 27°C the optimal temperature, they take 7 days. Importantly, at temperature above 29°C/30°C, no fruiting body is ever observed, while mycelium growth still proceeds up to 37°C.

As stated in the section on “The mycelium” in the chapter on “Morphology and Cytology”, an interesting feature of *P. anserina* fructification is the non-random repartition of the fruiting body on the mycelium, especially when grown on M2 medium. Indeed, on M2, the friendly mold differentiates perithecia mostly along a ring with an inner diameter of 2 cm and a width of 1 cm (figure 95). Such ring is reminiscent of the “fairy rings” produced by many basidiomycetes. This ring feature is typical of *P. anserina* and the other species of the *P. anserina* species complex may differentiate other types of repartition with or without an obvious ring pattern (see figure 19).

Ring differentiation is robust and occurs without fail on M2 provided that the cultures are not senescent (see the many figures showing *P. anserina* M2 *mat+ mat-* heterokaryotic cultures in this book, i.e., figures 3, 19, 36, 94, 95, 96 and 97). It is nonetheless affected by many factors including temperature, light, nutrients and genetic factors, the general trends being that the lower the fertility, the larger and more diffuse the ring (figure 96). However, this may not be so simple, as seen with the homedomain transcription factor mutants (figure 96). The most intriguing feature of the ring formation is the central zone devoid of perithecia (that is lacking in the *ΔPah7* mutants). Indeed, male and female gametes
appear to differentiate uniformly on the thallus. The outer zone can be explained if maturation of the first-produced perithecia inhibits further differentiation of additional fruiting bodies. Yet, there is nothing obvious that should impede differentiation of fruiting bodies within the central zone. Intriguingly, when the fungus is inoculated in two close points, the central zone takes the shape of googles (figure 96), suggesting an active mechanism to inhibit production in the central zone (if nothing would inhibit production, the shape should be two interlocked rings).

<figure><img src="image_101.png" /><figcaption>**Figure 96** Environmental and genetic influence of the non-random repartition of fruiting bodies in *P. anserina* thallus. Top, influence of the temperature; Middle, effect of inoculation point, light and carbon source (M4 contains crystalline cellulose); bottom, genetic control with the examples of three mutants inactivated for the genes *Pah1*, *Pah5* and *Pah7* encoding homedomain transcription factors.</figcaption></figure>

Little is known about the molecular pathways controlling both the amounts of perithecia and their repartition. However, the inositol phosphate pathway appears to be a major player as shown in other fungi. Indeed, in the previous section, I mentioned the *spod1* mutant affected in an inositol phosphate polykinase and showing impairment in differentiation of both the maternal and zygotic tissues of the perithecia. This mutant has an additional interesting phenotype: when crossed with the wild type by "confrontation arrosée", perithecia differentiate along a triangle pointing within the *spod1* thallus (figure 97). Additional experiments have shown that this pattern is due to diffusion of a factor promoting perithecia development, which is not the inositol phosphate polykinase enzyme, but possibly its reaction products (i.e., the inositol-(1,3,4,5,6)-pentaphosphates made from inositol-(1,4,5)-triphosphates).

Interestingly, addition of inositol in M2 increases drastically the amounts of developing perithecia (figure 97) up to such levels that they fail to mature (possibly due to lack of enough nutrients). Inositol cannot be
used as food source by the friendly mold, indicating a signaling role of inositol and its phosphates
derivatives, in accordance with the phenotypes of the *spod1* mutants.

Meiotic Drive Elements: Spore Killers

Meiotic Drive Elements are genetic loci that subvert the law of Mendel that posits equipartition of alleles/idiomorphs during meiosis by eliminating nuclei that do not contain them. Meiotic Drive Elements

<figure><img src="image_102.png" /><figcaption>**Figure 97** Involvement of inositol and inositol polyphosphates in perithecium production and repartition. Left: a cross between the *PaPks1-193* mutant lacking melanin and *spod1* produces a triangle of pigments and perithecia on the *spod1* thallus. The dark color of these perithecia shows that their maternal tissues are from *spod1* (for comparison, those on the *PaPks1-193* mutants lacking pigments have maternal tissues from *PaPks1-193* as expected). Right, addition of inositol in the M2 medium greatly increases perithecia production; these are smaller than on M2 because they fail to fully mature.</figcaption></figure>
<figure><img src="image_103.png" /><figcaption>**Figure 98** The *het-s/het-S* *P. anserina* spore killer. The spore killing phenomenon occurs at 18°C in early-produced asci when ascogonia from the *het-s* strain carrying the het-s prion are fertilized by male gametes carrying the *het-S* allele. Prion amyloids may then be present in early asci. If *het-s* and *het-S* are segregated during the first meiotic division, ascospores carrying two het-S nuclei will produce the het-S protein which in the presence of the het-s prion will promote a reaction killing the two het-S ascospores, while the two het-s ones survive and carry the prion. It is not clear what happens to second division segregation asci (SDS) of such crosses (do all the ascospores die?), but the phenomenon occurs in a minority of asci, indicating an inefficient transmission of the het-s prion, especially at temperature above 20°C where the phenomenon is not observed. Lack of spore killing in late-produced asci confirms this assumption: as the dikaryotic lineage produces croziers and asci, the het-s amyloids may be irreversibly lost, freeing asci from the presence of the prion.</figcaption></figure>

carry thus at least two activities: one that kills and the other one that enables resistance. In most investigated instances, these two activities are carried out by two different factors, encoded by two different loci that remained linked through meiosis (often thanks to the presence of genomic inversions that results in recombination inhibition). In fungi, meiotic products end up in meiospores (e.g., ascospores in the *Ascomycota*), meiotic drive element are thus called "Spore Killer".

Jean Bernet described the first Spore Killer ever in crosses between the *het-s* and *het-S* strains that we now know is related to the presence of the het-s prion and its interaction with the het-S protein (figure 98). Indeed, he observed that at low temperature (18°C) the asci produced early frequently contained two mature spores instead of the expected ones, in crosses involving the *het-s* strain (that we now know contains the het-s prion) as maternal parent and the *het-S* one as paternal parent. On the contrary, he did not observed the phenomenon when *het-s* was used as paternal parent and *het-S* as the maternal one, nor with the *het-s*\* strain (that we now know are devoid of prion). He also observed that the ascospores from the two-spored asci are het-s (and thus contain the prion) and not het-s\*. We now interpret easily Bernet's observations, through the maternal inheritance of the het-s prion that can only be transmitted by *het-s* ascogonia and its incompatible interaction in ascospores with the het-S protein in asci where the *het-s/het-S* alleles are segregated in first division (figure 98).
<figure><img src="image_104.png" /></figure>

**Figure 99** The T x S *P. anserina* spore killer. The spore killer action is observed in S x T crosses, which mostly produce two-spored asci, while S x S and T x T crosses yield the usual four-spores asci. Right, interpretation of the spore killer (in red) action by killing ascospores carrying only the sensitive allele/idiomorph (in yellow). Proportion of two-spored asci depends on the first segregation frequency of the Spore Killer locus and hence its chromosomal location: as seen on the left the T meiotic drive element is located close to its centromere resulting in more than 95% two-spored asci (one four-spored is shown for comparison in the S x T picture). Note that lethal mutations acting during ascospore formation will also yield two-spored asci. However, in such instance, surviving ascospores will carry a wild-type allele and upon further crosses these survivors will yield four-spored asci, contrary to spore killers that will always yield two-spored ones.

Jean Bernet described another Spore Killing phenomenon between the T and T' strains of "*P. anserina*". We now know that strain T, which contained the meiotic drive element, is a *P. comata* strain, while we don't know what was strain T'. Nevertheless, the spore killing effect can be seen in crosses between the T and S strains (figure 99). Identification of the locus responsible for the T x S led to the surprising discovery that both the survival and killing activities are carried out by a single gene called *Spok1*. This gene encodes for a protein with a nuclease and kinase domains responsible for killing and resistance, respectively. It conserved its activity when transferred into *Sordaria macrospora*. Surprisingly, the S strain also contains a *Spok* gene encoding a protein very similar to the Spok1 protein (87% identity between Spok1 and Spok2), called *Spok2*. *Spok2* is inactive in the presence of *Spok1*, but proved fully active in its absence. Two additional *Spok* genes, *Spok3* and *Spok4*, were discovered in some strains of *P. anserina* and in another strain of the *P. anserina* species complex, *P. pauciseta*. These also act as Spore Killers and interact in complex fashion with *Spok1*. Indeed, *Spok1* provides resistance also to *Spok3* and
*Spok4*, while *Spok4* provides resistance to *Spok1* and *Spok3* does not. Note that *Spok2*, *Spok3* and *Spok4* do not interact, i.e., do not inhibit their respective killing and do not provide resistance. All four genes account for the known complex Spore Killer patterns detected in *P. anserina* populations, but for the het-s/het-S one.

Owing to their distortion effect on meiosis, Spore Killers are preferentially transmitted to the progeny. Not surprisingly, het-s strains are twice as frequent as het-S ones and more than 90% of them naturally contain the het-s prion. In the case of the *Spok* genes, the full pattern of their presence in the various members of the *P. anserina* species complex is not known. The *Spok2* gene appears present in most strains of *P. anserina* and in the *P. pauciseta* strain that has been sequenced. On the contrary, *Spok1* is present only in the *P. comata* T strain, while *Spok3* and *Spok4* have an intermediate distribution.
Natural products biosynthesis

Since the release of the genome sequence of *P. anserina*, it has been realized that the friendly mold is able to produce compounds with industrial value. These may have use principally in pharmaceutical, remediation and biofuels technologies. Two major kinds of products are presently studied: secondary metabolites and enzymes.

Secondary metabolites

Genome analysis indicates that *P. anserina* may be able to produce nearly 40 secondary
metabolites, since its genome encodes that many secondary metabolites pathways (Figure 100).
Biochemical analyses have so far shown that the friendly mold synthesizes anserinones A and B, two
quinones with antifungal, antibacterial and anticancer activities. Additionally, one species of the *P.
anserina* species complex (unfortunately, we don't know which one, since the paper did not provide the
actual ITS sequence, but only states that it is 99% identical to that of the reference strain S) is able to
produce sterigmatocystin, secosterigmatocystin, and 13-hydroxyversicolorin B, a derivative of
anthraquinone. The sterigmatocystin produced by the friendly mold was shown to be able to efficiently
kill *Anopheles gambiae* mosquito larvae.

Most genes involved in secondary metabolite production are clustered as observed in other
fungi. Yet, the first analyzed pathway, the one enabling to produce dihydroxynaphtalene (DHN)-melanin,
has its genes scattered all over the genome. The production of DHN-melanin starts with a polyketide
synthase whose gene is located at the centromere of chromosome 2 (figure 100). The *PaPks1* gene has
many mutants, which are used in many genetical and cytological analyses (see Developmental genetics:
grafting and genetic mosaics). The rest of the genes involved in DHN-melanin synthesis have not been
thoroughly analyzed. However, some the laccases involved at the last step of polymerization of melanin
in ascospores have been identified. Surprisingly, they are not canonical laccases, and are related to
ascorbate oxidases and ferroxidases.
<table><thead><tr><th>Region</th><th>Type</th><th>From</th><th>To</th><th>Most similar known cluster</th><th>Similarity</th></tr></thead><tbody><tr><td>Region 1.1</td><td>NRPS-like, NRPS, T1PKS</td><td>1,796,876</td><td>1,878,895</td><td></td><td></td></tr><tr><td>Region 1.2</td><td>T1PKS</td><td>4,090,203</td><td>4,138,115</td><td></td><td></td></tr><tr><td>Region 1.3</td><td>terpene</td><td>5,383,359</td><td>5,405,264</td><td></td><td></td></tr><tr><td>Region 2.1</td><td>T1PKS</td><td>501,510</td><td>537,011</td><td>naphthalene</td><td>Polyketide</td><td>22%</td></tr><tr><td>Region 2.2</td><td>T1PKS</td><td>2,769,119</td><td>2,813,891</td><td></td><td></td><td></td></tr><tr><td>Region 2.3</td><td>T1PKS</td><td>2,933,411</td><td>2,979,798</td><td>sterigmatocystin</td><td>Polyketide</td><td>46%</td></tr><tr><td>Region 2.4</td><td>NRPS</td><td>3,069,555</td><td>3,120,058</td><td></td><td></td><td></td></tr><tr><td>Region 3.1</td><td>T1PKS</td><td>1,299,909</td><td>1,348,569</td><td></td><td></td><td></td></tr><tr><td>Region 3.2</td><td>NRPS</td><td>4,460,651</td><td>4,506,700</td><td>biotin</td><td>Other</td><td>66%</td></tr><tr><td>Region 4.1</td><td>T1PKS, NRPS-like</td><td>31,355</td><td>66,381</td><td></td><td></td><td></td></tr><tr><td>Region 4.2</td><td>indole</td><td>408,609</td><td>431,472</td><td></td><td></td><td></td></tr><tr><td>Region 4.3</td><td>NRPS-like</td><td>606,778</td><td>641,809</td><td></td><td></td><td></td></tr><tr><td>Region 4.4</td><td>T1PKS</td><td>1,547,198</td><td>1,596,340</td><td>solanapyrone D</td><td>Polyketide</td><td>33%</td></tr><tr><td>Region 4.5</td><td>T3PKS</td><td>1,991,727</td><td>2,032,583</td><td></td><td></td><td></td></tr><tr><td>Region 4.6</td><td>NRPS-like</td><td>3,569,794</td><td>3,607,322</td><td></td><td></td><td></td></tr><tr><td>Region 4.7</td><td>NRPS</td><td>3,674,808</td><td>3,737,150</td><td></td><td></td><td></td></tr><tr><td>Region 4.8</td><td>NRPS</td><td>3,756,520</td><td>3,811,587</td><td></td><td></td><td></td></tr><tr><td>Region 5.1</td><td>indole</td><td>272,223</td><td>286,753</td><td></td><td></td><td></td></tr><tr><td>Region 5.2</td><td>T1PKS</td><td>327,606</td><td>374,381</td><td>9-methylstreptimidone</td><td>Polyketide:Modular type I</td><td>6%</td></tr><tr><td>Region 5.3</td><td>indole</td><td>431,684</td><td>453,478</td><td></td><td></td><td></td></tr><tr><td>Region 5.4</td><td>T1PKS</td><td>473,503</td><td>519,108</td><td></td><td></td><td></td></tr><tr><td>Region 5.5</td><td>NRPS</td><td>700,654</td><td>743,925</td><td></td><td></td><td></td></tr><tr><td>Region 5.6</td><td>T1PKS</td><td>941,446</td><td>986,835</td><td></td><td></td><td></td></tr><tr><td>Region 5.7</td><td>NRPS, T1PKS</td><td>1,568,699</td><td>1,619,177</td><td>UNII-YC2Q1Q94PT</td><td>Polyketide</td><td>100%</td></tr><tr><td>Region 5.8</td><td>terpene</td><td>1,996,169</td><td>2,017,799</td><td>squalene statin S1</td><td>Terpene</td><td>40%</td></tr><tr><td>Region 5.9</td><td>NRPS-like</td><td>2,812,617</td><td>2,854,255</td><td></td><td></td><td></td></tr><tr><td>Region 5.10</td><td>T1PKS</td><td>2,890,310</td><td>2,930,372</td><td></td><td></td><td></td></tr><tr><td>Region 5.11</td><td>NRPS, T1PKS</td><td>3,093,531</td><td>3,146,847</td><td>phyllostictine A / phyllostictine B</td><td>NRP + Polyketide</td><td>40%</td></tr><tr><td>Region 5.12</td><td>T1PKS</td><td>3,338,185</td><td>3,378,460</td><td></td><td></td><td></td></tr><tr><td>Region 5.13</td><td>T1PKS</td><td>4,554,977</td><td>4,601,222</td><td></td><td></td><td></td></tr><tr><td>Region 6.1</td><td>T1PKS</td><td>14,818</td><td>48,227</td><td></td><td></td><td></td></tr><tr><td>Region 6.2</td><td>T3PKS, T1PKS</td><td>2,921,451</td><td>2,973,589</td><td></td><td></td><td></td></tr><tr><td>Region 6.3</td><td>T1PKS, NRPS</td><td>3,219,215</td><td>3,270,835</td><td></td><td></td><td></td></tr><tr><td>Region 6.4</td><td>NRPS-like</td><td>3,850,773</td><td>3,890,945</td><td></td><td></td><td></td></tr><tr><td>Region 6.5</td><td>NRPS</td><td>3,935,957</td><td>4,001,083</td><td></td><td></td><td></td></tr><tr><td>Region 6.6</td><td>T1PKS</td><td>4,020,000</td><td>4,068,750</td><td>solanapyrone D</td><td>Polyketide</td><td>33%</td></tr></tbody></table>

**Figure 100** Prediction of secondary metabolite clusters of *P. anserina* with antiSMASH. The fungal version of the antiSMASH prediction tool 5.0 identified 37 secondary metabolite gene clusters using the relaxed parameters. DHN-melanin biosynthesis is initiated by the polyketide synthase of the region 2.1 that produces naphtalene. The other genes involved in the melanin biosynthesis are not linked to region 2.1.

The second secondary metabolite pathway that has been characterized by molecular genetics analyses is the one predicted to produce sterigmatocystin, a toxic polyketid. It is thus most likely that sterigmatocystin and secosterigmatocystin detected by biochemical analyses are produced thanks to this cluster. It has been horizontally transferred from *Eurotiales* into the chromosome 2 of the genome of the ancestors of the *P. anserina*. Deletion of the cluster results in sensitivity to oxidative stress. Based on the genome analysis (figure 100), *P. anserina* has the ability to produce additional polyketides, but also non-
ribosomal peptides and terpene(s). It also likely synthesizes more complex compounds since its genome
encodes for proteins having fused polyketide and non-ribosomal peptide synthase domains.

In addition to the above-discussed secondary metabolites, *P. anserina* synthesizes various
oxylipins of the icosanoid and isoprostanoid families thanks to lipoxygenases and cyclooxygenases. These
are in turn transformed into organic volatile compounds, often with 8 carbons, that are used by the
fungus to repel nematodes.

Enzymes

The other natural products of industrial value made by *P. anserina* are enzymes. These may be
used directly or the genes that encode them are used to optimize production of natural compounds in
biotechnological application. An example of the latter is the use of a 3-dehydroshikimate dehydratase
gene to optimize the production of vanillin from glucose by *Schizosaccharomyces pombe*. Vanillin is an
aromatic aldehyde that is extensively used as a flavoring and aromatic agent in food, cosmetics, cleaning
products, etc. We don't know whether the optimized strains carrying the *P. anserina* enzyme are
presently used in industrial scale production of vanillin. Another example is the potential use of arylamine
N-acetyltransferases in detoxification of anilines. Indeed, *P. anserina* produce two such enzymes, one of
which is very efficient to acetylate anilines, including 3,4-dichloroanilin or DCA. DCA is a degradation
product of diuron, a widely used herbicide. DCA is highly toxic and contaminate many sites all over the
world. It was shown that adding the fungus to soil, contaminated in a way that prevent seed germination,
restores some health to the soil as to permit germination.

By far the most investigated enzymes in view of industrial applications are those involved in
biomass degradation or CAZYmes (figure 101). Indeed, analysis of the genome sequence has permitted to
discover a large array of genes involved in plant biomass degradation, including orthologues of genes
acting during lignin degradation in basidiomycetes. Biochemical analyses have confirmed that *P. anserina*
secretes indeed in the medium many enzymes having activities including cellulase, xylanase, pectinase,
arabinofuranosidase, arabinanase, galactanase, laccase and tyrosinase. Many enzymes encoded by these
genes are under scrutiny for their ability to enhance the enzymatic cocktails dedicated to breakdown the
complex lignocellulosic biomass into simple sugars for second-generation biofuel production.
*Trichoderma reesei*, the fungus used in industry to produce the cocktails, is an efficient cellulase
<figure><img src="image_105.png" /><figcaption>**Figure 101** *P. anserina* CAZYmes present in the CAZY database as of december 2019. Of note is the presence of numerous Auxilliary Activity enzymes potentially involved in lignin break down.</figcaption></figure>

producer, but is naturally endowed with surprisingly little diversity of enzymes. Cocktail supplementations with *P. anserina* enzymes produce in *Pichia* yeasts often confer greatly improved activity. Paramount for such a task are the *Lytic Polysaccharide Monoxygenases* or LPMOs. LPMOs can cleave by oxidation various polysaccharides, including cellulose, and have thus been reassigned from class GH61 to classes AA9, AA10, AA11 & AA13. The *P. anserina* genome encodes 33 LPMOs. Laccases and especially the thermostable billirubin-like ones are also promising enzymes to improve not only biomass degradation, but also to partake in the removal of toxic xenobiotics and some plastics. Note that in addition to the CAZYmes listed in figure 101, *P. anserina* also possesses over 110 cytochrome P450 genes, 9 peroxidases (not counting the catalases), many Glutathione S-transferases... All these enzymes may participate in lignocellulose and plastic breakdown and/or detoxification of noxious compounds.

It is worth mentioning, that while *Neurospora crassa* is now used as a model to understand the degradation of cellulose and its regulation, *P. anserina* is presently considered as a promising model to understand the complex process of lignocellulose breakdown by fungi, through the analyzes of both the penetration of biomass (see Appressorium-like structure differentiation) and the action of enzymes encoded by the CAZYmes genes, but also the other enzymes potentially participating in the process. *P. anserina* is able to complete its lifecycle on wood and it is thus easy to finely assess whether mutant have defects in scavenging nutrients from wood. Gene inactivation of all the laccase genes has already shown that many of those are necessary for growth on lignocellulose. Similarly, the genes encoding catalases are required for growth in the presence of lignin. On the contrary, many enzymes shown to be potent to degrade lignocellulose in basidiomycetes appear dispensable for the growth and fertility of *P. anserina* on
wood (at least in a laboratory setting).
## REFERENCES

Below are lists of papers, PhD dissertations, book chapters, etc., having *P. anserina* as one of its major subjects of study. Papers only mentioning studies with the friendly mold for reference are not listed.

### Herbarium Specimen

- Cesati, V. (1852). **1642. Sphaeria pauciseta. Klotzschii herbarium vivum mycologicum sistens fungorum per totam germaniam crescentium collectionem perfectam - Centuria XVII. L. Rabenhorst.**

- Cesati, V. (1857). **526. Malinvernia Rabenh. Klotzschii herbarium vivum mycologicum sistens fungorum per totam germaniam crescentium collectionem perfectam - Editio nova Series Prima Centuria VI. L. Rabenhorst.**

### Original Articles

- Unknown author (1852). "Sammlungen." *Botanische Zeitung* **10**: 285-288.

- Rabenhorst, L. (1857). "Erklärung der Taf. XV." *Hedwigia* **1**: 116 - pl. 115 fig.114.

- Winter, G. (1873). "Einige vorläufige Mittheilungen über di Gattung Sordaria." *Botanische Zeitung* **31**(1. august 1873): 481-485.

- Winter, G. (1873). "Die Deutschen Sordarien." *Abhandlungen der Naturf. Gesellschaft zu Halle* **13**: 1-43 + Taf. VII-XI.

- Spegazzini, C. (1880). "Fungi Argentini." *Anales de la Sociedad Científica Argentina* **10**: 5-33.

- Niessl (1883). "Ueber die Theilung der Gattung Sordaria." *Hedwigia* **22**: 153-156.

- Ellis, J. B. and B. M. Everhart (1888). "New Species of Fungi from Various Localities (Continued)." *The Journal of Mycology* **4**(8): 73-82.

- Spegazzini, C. (1899). "Fungí argentini novi v. critici." *Anales del Museo Nacional de Historia Natural de Buenos Aires Ser. 2* **6**: 289-365.

- Wolf, F. A. (1912). "Spore formation in *Podospora anserina* (Rahb.) Winter." *Annals of Mycology* **10**: 60-64.

- Satina, S. (1916). "Studies in the development of certain species of the sordariaceae." *Bulletin de la Société impériale des naturalistes de Moscou, nouvelle serie*, **30**: 106-142 Pl. 101-102.

- Chenantais, J. E. (1919). "Recherches sur les Pyrenomycètes (Suite et Fin)." *Bull. Soc. Mycol. Fr.* **35**: 113-139 & Pl. I-VI.

- Ames, L. M. (1930). "A study of some homothlic and heterothallic Ascomycetes." *Mycologia* **22**: 318-322.

- Dowding, E. S. (1931). "The sexuality of the normal, giant and dwarf spores of *Pleurage anserina*. (Ces) Kuntze." *Ann. Bot.* **45**: 1-14.

- Ames, L. M. (1932). "A hermaphrodite self-sterile condition in *Pleurage anserina*." *Bull. Torrey Botan. Club* **59**: 341-345.

- Ames, L. M. (1934). "Hermaphroditism involving self-sterility and cross-fertility in the ascomycete *Pleurage anserina*." *Mycologia* **26**: 392-414.

- Dodge, B. O. (1936). "Spermatia and nuclear migration in *Pleurage anserina*." *Mycologia* **28**: 284-291.

- Milovtzova, M. (1937). "Data on the microflora of Ukraine (in Ukrainian)." *Travaux de l'Institut de Botanique, Kharkov* **2**: 17-22.

- Page, W. M. (1939). "Contributions to the life History of certain coprophilous fungi." *Trans. Br. Mycol. Soc.* **23**: 253-268.

- Rizet, G. (1939). "De l'hérédité du caractère absence de pigment dans le mycélium d'un ascomycète du genre *Podospora*." *Comptes-Rendus de l'Académie des Sciences, Paris* **209**: 771-774.

- Rizet, G. (1940). "Sur les diverses formes de la distribution des "sexes" chez le *Podospora minuta*." *C. R. Soc. Biol. Paris* **133**: 31-32.

- Rizet, G. (1941). "Sur l'analyse génétique des asques du *Podospora anserina*." *C. R. Acad. Sci. Paris* **212**: 59-61.

- Rizet, G. (1941). "La ségrégation des sexes et de quelque caractère somatiques chez le *Podospora anserina*." *C. R. Acad. Sci. Paris* **213**: 42-45.

- Rizet, G. (1941). "La valeur génétique des périthèces nés sur des souches polycaryotiques chez le *Podospora anserina*." *Bull. Soc. Bot. France* **88**: 517-520.
- Rizet, G. (1941). "Quelques caractères remarquables des mutations observées chez le *Podospora anserina*." *C. R. Soc. Biol. Paris* **135**: 1080-1082.

- Rizet, G. (1941). "La formation d'asques hybrides dans les confrontations de souches "self-stériles" et de souches "self-fertiles" chez le *Podospora anserina*." *Rev. Mycologie* **6**: 128-133.

- Rizet, G. (1941). "Sur l'hérédité d'un caractère de croissance et du pouvoir germinatif des spores dans une lignée de l'Ascomycète *Podospora anserina*." *Bull. Soc. Linéenne de Norm. 9th ser.* **Sér. 2**: 131-136.

- Rizet, G. (1941). "Les résultats d'ordre génétique et le problème de la sexualité chez le *Podospora anserina*." *Rev. Mycologie* **7**: 97-100.

- Rizet, G. (1942). "Sur l'obtention d'irrégularités dans les asques et les spores de Pyrénomycètes du genre Podospora par l'action de quelques anasthèsiques." *Bull. Soc. Linéenne Norm.* **2**: 123-130.

- Rizet, G. (1943). "L'existence des races génétiques chez le *Podospora anserina*." *Bull. Soc. Linéenne Norm.* **3**: 14-15.

- Rizet, G. and C. Engelmann (1949). "Contribution à l'étude génétique d'un Ascomycète tétrasporé : *Podospora anserina* (Ces.) Rehm." *Revue de Cytologie et Biologie Végétale* **11**: 201-304.

- Rizet, G. (1950). "Sur le démasquage du géotype des souches $s^5$ de *Podospora anserina*." *C. R. Acad. Sci. Paris* **231**: 719-721.

- Rizet, G. and G. Delannoy (1950). "Sur la production par des hétérozygotes monofactoriels de *Podospora anserina* de gamétophytes phénotypiquement différents des gamétophytes parentaux." *C. R. Acad. Sci. Paris* **231**: 588-590.

- Rizet, G. and G. Sichler (1950). "Sur le camouflage durable du géotype chez *Podospora anserina*." *C. R. Acad. Sci. Paris* **231**: 630-631.

- Moreau, F. and M. Moreau (1951). "Observations cytologiques sur les Ascomycètes du genre Pleurage." *Revue de Mycologie* **16**: 198.

- Rizet, G. (1952). "Les phénomènes de barrage chez *Podospora anserina*. I. Analyse génétique des barrages entre souches S and s." *Rev. Cytol. Biol. Veg.* **13**: 51-92.

- Monnot, F. (1953). "Sur la localisation du gène S et sur quelques particularités du crossing-over chez *Podospora anserina*." *C. R. Acad. Sci. Paris* **236**: 2330-2332.

- Monnot, F. (1953). "Sur la possibilité de réaliser des croisements réciproques chez l'Ascomycète *Podospora anserina*." *C. R. Acad. Sci. Paris* **236**: 2263-2264.

- Rizet, G. (1953). "Sur la multiplicité des mécanismes génétiques conduisant à des barrages chez *Podospora anserina*." *C. R. Acad. Sci. Paris* **237**: 666-668.

- Rizet, G. (1953). "Sur l'impossibilité d'obtenir la multiplication végétative ininterrompue et illimitée de l'Ascomycète *Podospora anserina*." *C. R. Acad. Sci. Paris* **237**: 838-840.

- Rizet, G. (1953). "Sur la longévité des souches de *Podospora anserina*." *C. R. Acad. Sci. Paris* **237**: 1106-1109.

- Rizet, G. and K. Esser (1953). "Sur des phénomènes d'incompatibilité entre souches d'origines différentes chez *Podospora anserina*." *C. R. Acad. Sci. Paris* **237**: 760-761.

- Esser, K. (1954). "Sur le déterminisme génétique d'un nouveau type d'incompatibilité chez Podospora." *C. R. Acad. Sci. Paris* **238**: 1731-1733.

- Marcou, D. (1954). "Sur la longévité des souches de *Podospora anserina* cultivées à diverses températures." *C. R. Acad. Sci. Paris* **239**: 895-897.

- Marcou, D. (1954). "Sur le rajeunissement par le froid des souches de *Podospora anserina*." *C. R. Acad. Sci. Paris* **239**: 1153-1155.

- Tavlitzki, J. (1954). "Sur la croissance de *Podospora anserina* en milieu synthétique." *C. R. Acad. Sci. Paris* **238**: 2341-2343.

- Esser, K. (1955). "Genetische Untersuchungen an *Podospora anserina*." *Ber. Deut. Botan. Ges.* **68**: 143-144.

- Esser, K. (1956). "Wachtum, Fruchtkörper-und Pigmentbildung von *Podospora anserina* in synthetischen Nährmedien." *Compt. Rend. Lab. Carlsb. Sér. Physiol.* **26**: 103-116.

- Esser, K. (1956). "Gen-Mutaten von *Podospora anserina* (Ces.) Rehm mit männlicher Verhalten." *Naturwissenschaften* **43**: 284.

- Esser, K. (1956). "Die Incompatibilitätsbeziehungen zwischen geographischen Rassen von *Podospora anserina* (Ces.) Rehm. I. Genetische Analyse der Semi-Incompatibilität." *Zeitschrift Fur Induktive Abstammungs- Und Vererbungslehre* **87**: 595-624.

- Franke, G. (1957). "Die Cytologie der Ascusentwicklung von *Podospora anserina*." *Z. indukt. Abst. Vererbungslehre* **88**: 159-160.

- Marcou, D. (1957). "Rajeunissement et arrêt de croissance chez *Podospora anserina*." *C. R. Acad. Sci. Paris* **244**: 661-663.

- Rizet, G. (1957). "Les modifications qui conduisent à la sénescence chez *Podospora anserina* sont-elles de nature cytoplasmique?" *C. R. Acad. Sci. Paris* **244**: 663-665.

- Rizet, G., D. Marcou, et al. (1958). "Deux phénomènes d'hérédité cytoplasmique chez l'Ascomycète *Podospora anserina*." *Bull. Soc. Franc. Physiol. Veget.* **4**: 136-149.

- Schecroun, J. (1958). "Sur la réversion provoquée des souches $s^5$ en s chez *Podospora anserina*." *C. R. Acad. Sci. Paris* **246**(1268-1270).

- Esser, K. (1959). "Die Incompatibilitätsbeziehungen zwischen geographischen Rassen von *Podospora anserina* (Ces.) Rehm. III. Untersuchungen zur Genphysiologie der Barragebildung und der Semi-Incompatibilität." *Zeitschrift Fur Induktive Abstammungs Und Vererbungslehre* **90**: 445-456.
- Marcou, D. and J. Schecroun (1959). "La sénescence chez Podospora pourrait être due à des particules cytoplasmiques infectantes." C. R. Acad. Sci. Paris **248**: 280-283.

- Rizet, G. and J. Schecroun (1959). "Sur les facteurs cytoplasmiques associés au couple de gènes S-s chez le *Podospora anserina*." C. R. Acad. Sci. Paris **249**: 2392-2394.

- Schecroun, J. (1959). "Sur la nature de la différence cytoplasmique entre souches s and sS de *Podospora anserina*." C. R. Acad. Sci. Paris **248**: 1394-1397.

- Bernet, J., K. Esser, et al. (1960). "Sur la structure génétique de l'espèce *Podospora anserina* et sur l'intérêt de cette structure pour certaines recherches de génétique." C. R. Acad. Sci. Paris **250**: 2053-2055.

- Marcou, D. (1961). "Notion de longévité et nature cytoplasmique du déterminant de la sénescence chez quelques champignons." *Annales des Sciences Naturelles, Botaniques Paris Sér. 12*, **2**: 653-764.

- Beisson-Schecroun, J. (1962). "Incompatibilité cellulaire et interactions nucléocytoplasmiques dans les phénomènes de "barrage" chez le *Podospora anserina*." *Annales de Génétique* **4**: 4-50.

- Delay, C. (1962). "Observation sur l'infrastructure des jeunes hyphes du mycélium de *Podospora anserina* (Ascomycète)." C. R. Acad. Sci. Paris **254** (3): 3737-3739.

- Franke, G. (1962). "Versuche zur Genomverdoppelung des Ascomyceten *Podospora anserina*." Z. Vererbungsl. **93**: 109-117.

- Kuenen, R. (1962). "Crossover und Chromatiden-Interferenz bei *Podospora anserina* Rehm." Z. Vererbungsl. **93**: 66-108.

- Kuenen, R. (1962). "Ein Modell zur Analyse der Crossover-Interferenz." Z. Vererbungsl. **93**: 35-65.

- Nguyen, H. v. (1962). "Rôle des facteurs internes et externes dans la manifestation de rythmes de croissance chez l'ascomycète *Podospora anserina*." C. R. Acad. Sci. Paris **254**: 2646-2648.

- Bernet, J. (1963). "Action de la température sur les modifications de l'incompatibilité cytoplasmique et les modalités de la compatibilité sexuelle entre certaines souches de *Podospora anserina*." Ann. Sci. Natur. Bot. Paris **Ser. 12** **4**: 205-223.

- Bernet, J. (1963). "Sur les modalités d'expression de gènes pouvant conduire à une incompatibilité cytoplasmique chez le champignon *Podospora anserina*." C. R. Acad. Sci. Paris **256**: 771-773.

- Delay, C. (1963). "Observations inframicroscopiques sur le mycelium " senescent " du *Podospora anserina* (Ascomycète)." C. R. Acad. Sci. Paris **256**: 4721-4724.

- Esser, K. (1963). "Die Phenoloxydasen des Ascomyceten *Podospora anserina*. I. Identifizierung von Laccase und Tyrosinase beim Wildstamm." Arch. Mikrobiol. **46**: 217-226.

- Esser, K. (1963). "Die Wirkungsweise von Antiseren auf die Phenoloxydasen von *Podospora anserina*." Naturwissenschaften **50**: 576-577.

- Marcou, D. (1963). "Sur l'influence du mode d'association des gènes sur les propriétés de certains hétérocaryotes du *Podospora anserina*." C. R. Acad. Sci. Paris **256**: 768-770.

- Esser, K., S. Dick, et al. (1964). "Die Phenoloxydasen des Ascomyceten *Podospora anserina*. II. Reinigung und Eigenschaften der Laccase." Arch. Mikrobiol. **48**: 306-318.

- Weber, P. and K. Esser (1964). "Die Aminosäurezusammensetzung von Laccase aus *Podospora anserina*." Naturwissenschaften **51**: 491-492.

- Bernet, J. (1965). "Mode d'action des gènes de "barrage" et relation entre l'incompatibilité cellulaire et l'incompatibilité sexuelle chez *Podospora anserina*." Annales des Sciences Naturelles, Botaniques Paris **6**: 611-768.

- Esser, K. (1966). "Die Phenoloxydasen des Ascomyceten *Podospora anserina*. III. Quantitative und qualitative Enzymunterschiede nach Mutation an nicht gekoppelten Loci." Z. Vererbungsl. **97**: 327-344.

- Begueret, J. (1967). "Sur la répartition en groupes de liaison de gènes concernant la morphologie des ascospores chez le *Podospora anserina*." C. R. Acad. Sci. Paris **264**: 462-465.

- Bernet, J. (1967). "Les systèmes d'incompatibilité chez le *Podospora anserina*." C. R. Acad. Sci. Paris Sér. D265: 1330-1333.

- Bernet, J. and L. Belcour (1967). "Sur la possibilité de sélectionner des mutants de gènes d'incompatibilité chez le *Podospora anserina* et sur les propriétés des premières allèles obtenus." C. R. Acad. Sci. Paris Sér. D 265: 1536-1539.

- Marcou, D. (1967). "Sur la structure d'un locus complexe chez le *Podospora anserina* : les relations entre la carte génétique et la carte de complémentation." C. R. Acad. Sci. Paris **265**: 1962-1965.

- Marcou, D. and M. Picard (1967). "Sur l'intérêt du *Podospora anserina* pour l'étude des problèmes de la recombinaison." C. R. Acad. Sci. Paris **264**: 759-762.

- Nguyen, H. v. (1967). "Les relations intercellulaires au cours de la croissance en "vague" chez le *Podospora anserina*." C. R. Acad. Sci. Paris **264**: 280-283.

- Nguyen, H. v. (1967). "Etude de rythmes internes de croissance chez le *Podospora anserina*." Ann. Sci. Natur. Bot. Paris **9**: 257-360.

- Padieu, E. and J. Bernet (1967). "Mode d'action des gènes responsables de l'avortement de certains produits de la méiose chez l'Ascomycète *Podospora anserina*." C. R. Acad. Sci. Paris **264**: 2300-2303.

- Auvity, M. (1968). "Dominance apicale et sénescence chez le *Podospora anserina*." C. R. Acad. Sci. Paris **267**: 1705-1708.

- Beckett, A., R. Barton, et al. (1968). "Fine structure of the wall apendage formation in ascospores of *Podospora anserina*." J. Gen. Microbiol. **53**: 89-94.
- Beckett, A. and I. M. Wilson (1968). "Ascus cytology of *Podospora anserina*." *J. Gen. Microbiol.* **53**: 81-87.

- Bernet, J. and J. Begueret (1968). "Sur les propriétés et la structure des facteurs d'incompatibilité chez *Podospora anserina*." *C. R. Acad. Sci. Paris Sér. D* **266**: 716-719.

- Esser, K. (1968). "Phenoloxidases and morphogenesis in *Podospora anserina*." *Genetics* **60**: 281-288.

- Begueret, J. (1969). "Sur le mécanisme des réactions d'incompatibilité chez le *Podospora anserina*." *C. R. Acad. Sci. Paris* **269**: 458-461.

- Belcour, L. and J. Bernet (1969). "Sur la mise en évidence d'un gène dont la mutation supprime spécifiquement certaines manifestations d'incompatibilité chez le *Podospora anserina*." *C. R. Acad. Sci. Paris* **269**: 712-714.

- Bernet, J. and J. Labarère (1969). "Effet de la dihydrostreptomycine sur l'incompatibilité chez le champignon *Podospora anserina*." *C. R. Acad. Sci. Paris* **269**: 59-62.

- Blaich, R. and K. Esser (1969). "Der cis-trans-Positionseffekt in Heterokaryon morphologischer Mutanten von *Podospora anserina*." *Arch. Mikrobiol.* **68**: 201-209.

- Chevaugeon, J. and H. Nguyen van (1969). "Internal determinism of hyphal growth rhythms." *Trans. Br. Mycol. Soc.* **53**: 1-14.

- Esser, K. (1969). "The influence of pH on rhythmic mycelial growth in *Podospora anserina*." *Mycologia* **61**: 1008-1011.

- Esser, K. (1969). "An introduction to *Podospora anserina*." *Neurospora Newsl.* **15**: 27-31.

- Herzfeld, F. and K. Esser (1969). "Die phenoloxydasen des Ascomyceten *Podospora anserina*. IV. Reinigung und Eigenschaften der Tyrosina." *Arch. Mikrobiol.* **65**(146-162).

- Holliday, R. (1969). "Errors in protein synthesis and clonal senescence in fungi." *Nature* **221**: 1224-1228.

- Marcou, D. (1969). "Sur la nature des recombinaisons intracistroniques et sur leurs répercussions sur la ségrégation de marqueurs extérieurs chez le *Podospora anserina*." *C. R. Acad. Sci. Paris* **269**: 2362-2365.

- Mirza, J. H. and R. F. Cain (1969). "Revision of the genus *Podospora*." *Canadian Journal of Botany* **47**: 1999-2048.

- Auvity, M. (1970). "Phytomorphogénèse : synthèse protéiques et ramification du mycelium du *Podospora anserina*." *C. R. Acad. Sci. Paris* **270**: 934-937.

- Blaich, R. (1970). "Somatishe Rekombination in einem Heterokaryon des Ascomyceten *Podospora anserina*." *Naturwissenschaften* **57**: 47.

- Blaich, R. and K. Esser (1970). "The incompatibility relationships between geographical races of *Podospora anserina*. IV. Biochemical aspects of the heterogenic incompatibility." *Molec. Gen. Genet.* **109**: 186-192.

- Esser, K. and W. Minuth (1970). "The phenoloxidases of the ascomycete *Podospora anserina*. VI Genetic regulation of the formation of laccase." *Genetics* **64**: 441-458.

- Hodgkiss, I. J. and R. Harvey (1970). "Effects of humidity and rainfall on spore discharge rythms in pyrenomycètes." *Trans. Br. Mycol. Soc.* **54**: 379-388.

- Lewis, C. M. and R. Holliday (1970). "Mistranslation and ageing in neurospora." *Nature* **228**: 877-880.

- Lysek, G. and K. Esser (1970). "Rhythmic mycelial growth in *Podospora anserina*. I. The pleiotropic phenotype of a mutant is caused by a point mutation." *Arch. Mikrobiol.* **73**: 224-230.

- Molitoris, H. P. and E. K. (1970). "Die phenoloxidasen des Ascomyceten *Podospora anserina*. V. Eigenschaften der Laccase I nach weiterer Reinigung." *Arch. Mikrobiol.* **72**(267-296).

- Picard, M. (1970). "Sur les données génétiques suggérant l'existence d'une unité de transcription polycistronique au sein du locus 14 chez le *Podospora anserina*." *C. R. Acad. Sci. Paris* **270**: 498-501.

- Toure, B. and D. Marcou (1970). "Nature, dimension et limites des évènements de recombinaisons génétiques à l'intérieur d'une unité de transcription polycistronique chez le *Podospora anserina*." *C. R. Acad. Sci. Paris* **270**: 619-621.

- Webster, J. (1970). "Coprophilous Fungi." *Trans. Br. Mycol. Soc.* **54**: 161-180.

- Zicler, D. (1970). "Division Spindle and Centrosomal Plaques during Mitosis and Meiosis in some ascomycetes." *Chromosoma* **30**: 287-304.

- Belcour, L. (1971). "Mode d'action des gènes d'incompatibilité chez le *Podospora anserina*. I. Analyse de deux mutations à effet pléitrope." *Molec. Gen. Genet.* **112**: 263-274.

- Bernet, J. (1971). "Sur un cas de suppression de l'incompatibilité cellulaire chez le champignon *Podospora anserina*." *C. R. Acad. Sci. Paris* **273**: 1120-1122.

- Blaich, R. and K. Esser (1971). "The incompatibility relationships between geographical races of *Podospora anserina*. V. Biochemical characterization of heterogenic incompatibility on cellular level." *Molec. Gen. Genet.* **111**: 265-272.

- Esser, K. (1971). "Breeding systems in fungi and their significance for genetic recombination." *Molec. Gen. Genet.* **110**: 86-100.

- Esser, K. and W. Minuth (1971). "The phenoloxidases of the Ascomycete *Podospora anserina*. IX. Microheterogeneity of laccase II." *Europ. J. Biochem.* **23**: 484-488.

- Hodgkiss, I. J. and R. Harvey (1971). "Factors affecting fruiting of *Pleurage anserina* in culture." *Transactions of the British Mycological Society* **57**: 533-536.

- Hodgkiss, I. J. and R. Harvey (1971). "Effects of temperature on spore discharge rhythms in pyrenomycetes." *Transactions of the British Mycological Society* **56**(2): 225-234.
- Larpent, J. P., M. Auvity, et al. (1971). "Croissance, ramification et différenciation cellulaire du thalle des Champignons." *Bulletin de la Société Botanique de France* **118**(sup1): 5-18.

- Lysek, G. (1971). "Rhythmic mycelial growth in *Podospora anserina*. III. Effect of metabolic inhibitors." *Arch. Mikrobiol.* **78**: 330-340.

- Lysek, G. (1971). "Rhythmische Wuchsformen bei höheren Pilzen." *Präparator* **17**: 105-111.

- Lysek, G. and K. Esser (1971). "Rhythmic mycelial growth in *Podospora anserina*. II. Evidence for a correlation with carbohydrate metabolism." *Arch. Mikrobiol.* **75**: 360-373.

- Molitoris, H. P. and K. Esser (1971). "The phenoloxidases of the Ascomycete *Podospora anserina*. VII. Quantitative changes in the spectrum of phenoloxidases during growth in submerged culture." *Arch. Mikrobiol.* **77**: 99-110.

- Picard, M. (1971). "Genetic evidence for a polycistronic unit of transcription in the complex locus "14" in *Podospora anserina*. I. Genetic and complementation maps." *Molec. Gen. Genet.* **111**: 35-50.

- Schanel, L. and K. Esser (1971). "The phenoloxidases of the Ascomycete *Podospora anserina*. VIII. Substrate specificity of laccase with different molecular structures." *Arch. Mikrobiol.* **77**: 111-117.

- Begueret, J. (1972). "Protoplasmic incompatibility: possible involvement of proteolytic enzymes." *Nat New Biol* **235**(54): 56-58.

- Bornefeld, T. and G. Lysek (1972). "Rhythmic Mycelial Growth in *Podospora anserina*. V. The Levels of Phosphorylated Intermediates." *Arch. Mikrobiol.* **87**: 119-128.

- Esser, K. (1972). "Genetic and biochemical analysis of rhythmically grown mycelia in the Ascomycete *Podospora anserina*." *J. Interdiscipl. Cycle Res.* **3**: 123-128.

- Esser, K. and W. Minuth (1972). "Abnormal cell wall structure in rhythmically growing mycelia of *Podospora anserina*." *Cytobiol.* **5**: 319-322.

- Esser, K. and H. Prillinger (1972). "A new technique to use spermatia for the production of mutants in *Podospora*." *Mutation Research* **16**: 417-419.

- Furuya, K. and S. I. Udagawa (1972). "Coprophilous pyrenomycetes from Japan I." *J. gen. Appl. Microbiol.* **18**: 433-454.

- Hodgkiss, I. J. and R. Harvey (1972). "Effect of carbon dioxide on the growth and sporulation of certain coprophilous ascomycètes." *Trans. Br. Mycol. Soc.* **59**: 409-418.

- Lysek, G. (1972). "Rhythmisches Mycelwachstum bei *Podospora anserina*. IV. Rhythmischer Verlauf der Trockengewichtsproduktion." *Arch. Mikrobiol.* **81**: 221-233.

- Lysek, G. (1972). "Rhythmic Mycelial Growth in *Podospora anserina*. VI. An Attempt to Elucidate the Growth Pattern of a Clock Mutant." *Arch. Mikrobiol.* **87**: 129-137.

- Melendez-Howell, L. M. (1972). "Le pore germinatif ascosporal dans le genre *Podospora* Ces." *Ann. Sci. Natur. Bot. Paris* **Ser. 12**, **13**: 129-140.

- Molitoris, H. P. (1972). "Zur struktur der Laccasen des Ascomyceten *Podospora anserina*." *Hoppe-Seyler's Z. Physiol. Chem.* **353**: 736.

- Molitoris, H. P., J. F. L. v. Breemen, et al. (1972). "The phenoloxidases of the Ascomycete *Podospora anserina*. X. Electron microscopic studies on the structure of laccases I, II and III." *Biochim. Biophys. Acta* **281**: 286-291.

- Simonet, J. M. and D. Zickler (1972). "Mutations affecting meiosis in *Podospora anserina*. I. Cytological studies." *Chromosoma* **37**: 327-351.

- Touré, B. (1972). "Double reversal of gene conversion polarity and multiple conversion events in the locus "14" in *Podospora anserina*." *Molec. Gen. Genet.* **117**: 267-280.

- Touré, B. and M. Picard (1972). "Consequences of double crossover detections on the functional interpretation of segment "29" in *Podospora anserina*." *Genet Res Camb* **19**: 313-319.

- Begueret, J. and J. Bernet (1973). "Proteolytic enzymes and protoplasmic incompatibility in *Podospora anserina*." *Nat New Biol* **243**(124): 94-96.

- Bernet, J., J. Begueret, et al. (1973). "Incompatibility in the fungus *Podospora anserina*." *Molec. gen. Genet.* **124**: 35-50.

- Labarere, J. (1973). "Propriété d'un système d'incompatibilité chez le champignon *Podospora anserina* et intérêt de ce système pour l'étude de l'incompatibilité." *C. R. Acad. Sci. Paris* **276**: 1301-1304.

- Molitoris, H. P. and B. Reinhammar (1973). "Elektronenspinresonanz-und Absorptionsspektren der Laccasen des Ascomyceten *Podospora anserina*." *Hoppe-Seyler's Z. Physiol. Chem.* **354**: 219-220.

- Picard, M. (1973). "Genetic evidence for a polycistronic unit of transcription in the complex locus "14" in *Podospora anserina*. II. Genetic analysis of informational suppressors." *Genet Res Camb* **21**: 1-15.

- Simonet, J. M. (1973). "Mutations affecting meiosis in *Podospora anserina*. Effect of mei2 mutants and recombination." *Molec. Gen. Genet* **123**: 263-281.

- Smith, J. R. and J. Rubenstein (1973). "The development of "senescence" in *Podospora anserina*. Journal of general microbiology." *Journal of general microbiology* **76**: 283-296.

- Smith, J. R. and J. Rubenstein (1973). "Cytoplasmic inheritance of the timing of "senescence" in *Podospora anserina*. Journal of general microbiology **76**: 297-304.
- Boucherie, H. and J. Bernet (1974). "Protoplasmic incompatibility and female organ formation in *Podospora anserina*: properties of mutations abolishing both processes." *Molec. gen. Genet.* **135**: 163-174.

- Labarere, J., J. Begueret, et al. (1974). "Incompatibility in *Podospora anserina*: comparative properties of the antagonistic cytoplasmic factors of a nonallelic system." *J. Bacteriol* **120**(2): 854-860.

- Lysek, G. and V. H. Witsch (1974). "Lichtabhängige Zonierungen bein Pilzen und ihre physiologischen Grundlagen." *Ber. Deut. Bot. Ges.* **87**: 207-213.

- Belcour, L. (1975). "Cytoplasmic mutations isolated from protoplasts of *Podospora anserina*." *Genet Res Camb* **25**: 155-161.

- Molitoris, H. P. and B. Reinhammar (1975). "The phenoloxidases of the ascomycete *Podospora anserina*. XI. The state of copper of laccases I, II and III." *Biochim. Biophys. Acta* **386**: 495-502.

- Belcour, L. (1976). "Loss of a cytoplasmic determinant through formation of protoplasts in *Podospora*." *Neurospora Newslet.* **23**: 26-27.

- Boucherie, H., J. Begueret, et al. (1976). "The molecular mechanism of protoplasmic incompatibility and its relationship to the formation of protoperithecia in *Podospora anserina*." *J. gen. Microbiol.* **92**: 59-66.

- Boucherie, H., Y. M. Delettre, et al. (1976). "A constitutive mutation in a posttranscriptional regulator gene for a phenoloxidase and proteases in *Podospora anserina*." *Biochem. Gen.* **14**: 857-868.

- Delettre, Y. M. and J. Bernet (1976). "Regulation of proteolytic enzymes in *Podospora anserina*: selection and properties of self-lysing mutant strains." *Molec. gen. Genet.* **144**: 191-197.

- Esser, K. and W. Keller (1976). "Genes inhibiting senescence in the ascomycete *Podospora anserina*." *Molec. gen. Genet.* **144**: 107-110.

- Kemp, R. F. O. (1976). "A new interpretation of unilateral nuclear migration in fungi with special reference to *Podospora anserina*." *Trans. Br. Mycol. Soc.* **66**: 1-5.

- Lysek, G. (1976). "Formation of perithecia in colonies of *Podospora anserina*." *Planta* **133**: 81-83.

- Mai, S. H. (1976). "Morphological studies in *Podospora anserina*." *Amer. J. Bot.* **63**: 821-825.

- Molitoris, H. P. (1976). "Die Laccasen des ascomyceten *Podospora anserina*. Beitrage zur Kenntnis von Struktur und Funktion eines Systems multiplier Enzyme." *Bibliotheca Mycologica Band* **52**: J. Cramer, Vaduz.

- Picard-Bennoun, M. (1976). "Genetic evidence for roboromal antisuppressors in *Podospora anserina*." *Molec. gen. Genet.* **147**: 299-306.

- Prillinger, H. (1976). "Genetische Kontrolle der Phenoloxydase laccase des Ascomyceten *Podospora anserina*. Dissert. Bochum." *Bibliotheca Mycologica* **51**.

- Simonet, J. M. (1976). "UV and γ-ray sensitivity of meiosis deficient mutants in *Podospora anserina*." *Mutat Res* **41**: 225-232.

- Begueret, J., M. Perrot, et al. (1977). "Ribosomal proteins in the fungus *Podospora anserina*: evidence for an electrophoretically altered 60S protein in a cycloheximide resistant mutant." *Mol Gen Genet* **156**(2): 141-144.

- Belcour, L. and O. Begel (1977). "Mitochondrial genes in *Podospora anserina*: recombination and linkage." *Mol Gen Genet* **153**(1): 11-21.

- Boucherie, H. and J. Bernet (1977). "Intracellular and extracellular phenoloxidases in the fungus *Podospora anserina*: effect of a constitutive mutation in a gene involved in their posttranscriptional control." *Molec. gen. Genet.* **157**: 53-59.

- Coppin-Raynal, E. (1977). "Ribosomal suppressors and antisuppressors in *Podospora anserina*: resistance to cycloheximide." *J. Bacteriol* **131**(3): 876-883.

- Esser, K. and P. Tudzynski (1977). "The prevention of senescence in the ascomycete *Podospora anserina* by the antibiotic Tiamulin." *Nature* **265**: 454-456.

- Hoffmann, P. and K. Esser (1977). "The phenoloxidases of the ascomycete *Podospora anserina*. XII. Affinity of laccases II and III to substrates with different substitution patterns." *Arch. Microbiol.* **112**: 111-114.

- Labarere, J. and B. J. (1977). "Protoplasmic incompatibility and cell lysis in *Podospora anserina*. I. Genetic investigations on mutations of a novel modifier gene that suppresses cell destruction." *Genetics* **87**: 249-257.

- Lysek, G. (1977). "Role of nutrition on the banding of fungi." *Trans. Br. Mycol. Soc.* **69**: 154-156.

- Perrot, M. and J. Begueret (1977). "Quantitative variation of a 60S ribosomal protein during growth of the fungus *Podospora anserina*." *Biochimie Tome* **59 n°10**: 799-804.

- Picard-Bennoun, M. and E. Coppin-Raynal (1977). "Une fonction ribosomique essentielle : le contrôle de la fidélité de la traduction." *Physiol. Veg.* **15**: 481-489.

- Prillinger, H. and K. Esser (1977). "The phenoloxidases of the ascomycete *Podospora anserina*. XIII. Action and interaction of genes controlling the formation of laccase." *Molec. gen. Genet.* **156**: 333-345.

- Tudzynski, P. and K. Esser (1977). "Inhibitors of mitochondrial function prevent senescence in the ascomycete *Podospora anserina*." *Molec. gen. Genet.* **153**: 111-113.

- Belcour, L. and O. Begel (1978). "Lethal mitochondrial genotypes in *Podospora anserina*: a model for senescence." *Molec. gen. Genet.* **163**: 113-123.

- Belcour, L., O. Begel, et al. (1978). "Four mitochondrial loci in *Podospora anserina*." *Neurospora NewsI* **25**: 26-27.
- Boucherie, H. and J. Bernet (1978). "Protoplasmic incompatibility and self-lysis in *Podospora anserina*: enzyme associated with cell destruction." *Can. J. Botany* **56**: 2171-2176.

- Crouzet, M. and J. Begueret (1978). "Cold-sensitivity of a double mutant strain combining two ribosomal mutations in the ascomycete *Podospora anserina*." *Molec. gen. Genet.* **165**: 283-288.

- Crouzet, M., M. Perrot, et al. (1978). "Genetic and biochemical analysis of cycloheximide resistance in the fungus *Podospora anserina*." *Biochem. Genet.* **16**(3-4): 271-286.

- Cummings, D. J., L. Belcour, et al. (1978). "Etude au microscope électronique du DNA mitochondrial de *Podospora anserina* et présence d'une série multimérique de molécules circulaires de DNA dans des cultures sénescentes." *C. R. Acad. Sci. Paris* **287**: 157-160.

- Delettre, Y. M., H. Boucherie, et al. (1978). "Protoplasmic incompatibility and cell lysis in *Podospora anserina*: effect of B-phenylpyruvic acid." *Biochemie und Physiol. der Pflanzen* **172**: 27-34.

- Labarere, J. and J. Bernet (1978). "A mutation inhibiting protoplasmic incompatibility in *Podospora anserina* that suppresses an extracellular laccase and protoperithecium formation." *J. gen. Microbiol.* **109**: 187-189.

- Minuth, W., M. Klischies, et al. (1978). "The phenoloxidases of the ascomycete *Podospora anserina*. XIV. Structural differences between high and low molecular weight laccases." *Eur. J. Biochem.* **90**: 73-82.

- Munkres, K. D. and R. S. Rana (1978). "Antioxidants prolong life span and inhibit the senescence-dependent accumulation of fluorescent pigment (lipofuscin) in clones of *Podospora anserina* s.+." *Mech Ageing Dev* **7**: 407-415.

- Simonet, J. M. and D. Zickler (1978). "Genes involved in caryogamy and meiosis in *Podospora anserina*." *Molec. gen. Genet.* **162**: 237-242.

- Stahl, U. and K. Esser (1978). "Inconsistency in the species concept for yeasts due to mutations during vegetative growth." *Europ. J. Appl. Biotechn.* **8**(271-278).

- Stahl, U., P. A. Lemke, et al. (1978). "Evidence for plasmid like DNA in a filamentous fungus, the ascomycete *Podospora anserina*." *Molec. gen. Genet.* **162**: 341-343.

- Barreau, C. and J. Begueret (1979). "Isolation and partial characterization of the multiple forms of deoxyribonucleic acid-dependent ribonucleic acid polymerase in the fungus *Podospora anserina*." *J. Biol. Chem.* **254**: 11566-11569.

- Belcour, L. and O. Begel (1979). "Le facteur cytoplasmique d'incompatibilité S de *Podospora anserina* n'est pas porté par les mitochondries." *C. R. Acad. Sci. Paris* **289**: 663-666.

- Boucherie, H. and J. Bernet (1979). "Relationship between the Mutant Trait of Self-Lysis and the Phenomenon of Cell Death in the Fungus *Podospora anserina*." *Gerontol.* **25**: 160.

- Cummings, D. J., L. Belcour, et al. (1979). "Mitochondrial DNA from *Podospora anserina*. II. Properties of mutant DNA and multimeric circular DNA from senescent cultures." *Mol Gen Genet* **171**(3): 239-250.

- Cummings, D. J., L. Belcour, et al. (1979). "Mitochondrial DNA from *Podospora anserina*. I. Isolation and characterization." *Mol Gen Genet* **171**(3): 229-238.

- Durrens, P., F. Laigret, et al. (1979). "*Podospora anserina* mutant defective in protoperithecium formation, ascospore germination, and cell regeneration." *J Bacteriol* **140**(3): 835-842.

- Esser, K., F. Saleh, et al. (1979). "Genetics of fruit body production in higher basidiomycetes. II. Monokaryotic and dikaryotic fruiting in Schizophyllum commune." *Curr Genet* **1**: 85-88.

- Esser, K. and P. Tudzynski (1979). "Genes and mitochondrial inhibitors preventing senescence in the ascomycete *Podospora anserina*." *Gerontol.* **25**: 163.

- Hahn, M. L., G. Lysek, et al. (1979). "Isolierung und Untersuchung spontaner Resistenzmutanten von *Podospora anserina*." *Angew. Botanik* **53**: 83-90.

- Labarere, J. and J. Bernet (1979). "Protoplasmic incompatibility in *Podospora anserina*: a possible role for its associated proteolytic activity." *Genetics* **93**: 525-537.

- Labarere, J. and J. Bernet (1979). "A pleiotropic mutation affecting protoperithecium formation and ascospore outgrowth in *Podospora anserina*." *J. Gen. Microbiol.* **113**: 19-28.

- Marcou, D. (1979). "Dominant enhancer effect of the meiotic mei4 mutant on recombination frequencies restricted to linkage group VI in *Podospora anserina*." *Mol Gen Genet* **173**(3): 299-305.

- Marcou, D., A. Masson, et al. (1979). "Evidence for non-random spatial distribution of meiotic exchanges in *Podospora anserina*: comparison between linkage groups 1 and 6." *Mol Gen Genet* **176**(1): 67-79.

- Marcou, D. and A. Raynal (1979). "Cytoplasmic Determinism of Longevity and Senescence in the Fungus *Podospora anserina*." *Gerontol.* **25**: 168.

- Raynal, A. (1979). "Evidence for a common cytoplasmic determinant of longevity and senescence in the ascomycete *Podospora anserina*." *Molec. Gen. Genet.* **175**: 281-292.

- Raynal, A. and L. Belcour (1979). "La senescence de *Podospora anserina*: un modele expérimental pour l'étude du vieillissement." *Symbioses Vol. XI Number 4*: 20 pp.
- Simonet, J. M. and D. Zickler (1979). "Linkage group-chromosome correlation in *Podospora anserina*." *Molec. Gen. Genet.* **175**: 359-367.

- Stahl, U. and K. Esser (1979). "Subsequent transfers of yeast may lead via single mutations to alterations of the species." *Biotechn. Letters* **1**: 383-385.

- Stahl, U., P. Tudzynski, et al. (1979). "Plasmid-like DNA in senescent cultures of the ascomycetous fungus *Podospora anserina*." *Physiol. Chem.* **360**: 1045.

- Tudzynski, P. and K. Esser (1979). "Chromosomal and extrachromosomal control of senescence in the ascomycete *Podospora anserina*." *Molec. Gen. Genet.* **173**: 71-84.

- Zickler, D. and J. M. Simonet (1979). "Mutations induites et analyse de la meiose." *Bull. Soc. Bot. Fr.*, **125**, *Actual. bot.* **2**: 33-38.

- Belcour, L. and O. Begel (1980). "Life-span and senescence in *Podospora anserina*: Effect of mitochondrial genes and functions." *J. Gen. Microbiol.* **119**: 505-515.

- Boucherie, E. and J. Bernet (1980). "Protoplasmic incompatibility in *Podospora anserina*: a possible function for incompatibility genes." *Genetics* **96**: 399-411.

- Coppin-Raynal, E. (1980). "Analytical chromotography of ribosomal proteins in the fungus *Podospora anserina*." *Anal. Biochem.* **109**: 395-398.

- Crouzet, M. and J. Begueret (1980). "Altered ribosomal proteins in mutants of the fungus *Podospora anserina*." *J Biol Chem* **255**(11): 4996-4999.

- Crouzet, M. and J. Begueret (1980). "A new mutant form of the ribosomal protein L21 in the fungus *Podospora anserina*: identification of the structural gene for this protein." *Mol Gen Genet* **180**(1): 177-183.

- Dequard, M., J. L. Couderc, et al. (1980). "Search for ribosomal mutants in *Podospora anserina*: genetic analysis of mutants resistant to paromomycin." *Biochem Genet* **18**(3-4): 263-280.

- Esser, K. and D. Graw (1980). "Homokaryotic fruiting in the bipolar-incompatible ascomycete *Podospora anserina*." *Mycologia* **72**: 534-541.

- Esser, K., P. Tudzynski, et al. (1980). "A model to explain senescence in the filamentous fungus *Podospora anserina* by the action of plasmid like DNA." *Molec. Gen. Genet.* **178**: 213-216.

- Furuya, K. and A. Naito (1980). "Stimulation of ascospore germination by phenolic compounds in memebres of the Sordariaceae." *Trans Mycol Soc Japan* **21**: 77-85.

- Jamet-Vierny, C., O. Begel, et al. (1980). "Senescence in *Podospora anserina*: amplification of a mitochondrial DNA sequence." *Cell* **21**(1): 189-194.

- Labarere, J. (1980). "Proteolytic activities during growth and aging in the fungus *Podospora anserina*: effects of specific mutations." *Arch. Microbiol.* **124**: 269-274.

- Picard-Bennoun, M. and D. Le Coze (1980). "Search for ribosomal mutants in *Podospora anserina*: genetic analysis of cold-sensitive mutants." *Genet Res Camb* **36**(3): 289-297.

- Raynal, A. (1980). "Relationships between mitochondria and longevity determinants in the ascomycete *Podospora anserina*." *Exp Mycol* **4**: 48-55.

- Simonet, J. M., D. Marcou, et al. (1980). "Chromosome map and preferential localization of meiotic exchanges in *Podospora anserina*." *unpublished*.

- Stahl, U. (1980). "Hybridisierung von Pilzen." *Grundlagen-Methoden-Anwendung. Habil. Bochum*.

- Stahl, U., U. Kuck, et al. (1980). "Characterization and cloning of plasmid like DNA of the ascomycete *Podospora anserina*." *Mol Gen Genet* **178**(3): 639-646.

- Tudzynski, P., U. Stahl, et al. (1980). "Transformation to senescence with plasmid like DNA in the ascomycete *Podospora anserina*." *Curr Genet* **2**: 181-184.

- Tudzynski, P., U. Stahl, et al. (1980). "Senescence in *Podospora anserina*." *The Gerontologist* **20**: N° 5 Part II, 215.

- Zickler, D. and J. M. Simonet (1980). "Identification of gene-controlled steps of ascospore development in *Podospora anserina*." *Exp Mycol* **4**: 191-206.

- Asselineau, D., J. Bernet, et al. (1981). "Protoplasmic incompatibility in *Podospora anserina*: possible involvement of the plasma membrane in the trigger mechanism." *J. Gen. Microbiol.* **25**: 139-146.

- Belcour, L. (1981). "Mitochondrial DNA and senescence in *Podospora anserina*." *Curr Genet* **4**: 81-82.

- Belcour, L., O. Begel, et al. (1981). "Mitochondrial DNA amplification in senescent cultures of *Podospora anserina*: variability between the retained amplified sequences." *Curr Genet* **3**: 13-21.

- Boucherie, H., C. H. Dupont, et al. (1981). "Polypeptide synthesis during protoplasmic incompatibility in the fungus *Podospora anserina*." *Biochim Biophys Acta* **653**(1): 18-26.

- Coppin-Raynal, E. (1981). "Ribosomal suppressors and antisuppressors in *Podospora anserina*: altered susceptibility to paromomycin and relationships between genetic and phenotypic suppression." *Biochem Genet* **19**(7-8): 729-740.

- Dequard, M. and L. Belcour (1981). "Impairment of cytoplasmic protein synthesis can be detected on whole cells by cytochrome spectra." *Exp Mycol* **5**: 363-368.
- Durrens, P. (1981). "The phenoloxidases of the ascomycete *Podospora anserina*: the three forms of the major laccase activity." *Arch. Mikrobiol.* **130**: 121-124.

- Kuck, U., U. Stahl, et al. (1981). "Plasmid like DNA is part of mitochondrial DNA in *Podospora anserina*." *Curr Genet* **3**: 151-156.

- Lysek, G. and K. Schrüfer (1981). "Wuchsrhythmen (banding) bei *Podospora anserina* (Ascomycetes): Wirkung von Alkali-Ionen." *Ber. Deut. Bot. Ges.* **94**: 105-112.

- Perrot, M. and J. Begueret (1981). "Genetics of ribosomal components in Podospora spp. as revealed by interspecific hybridization." *J Bacteriol* **145**(1): 82-87.

- Picard-Bennoun, M. (1981). "Mutations affecting translational fidelity in the eukaryote *Podospora anserina*: characterization of two ribosomal restrictive mutations." *Mol Gen Genet* **183**(1): 175-180.

- Picard-Bennoun, M. and J. Begueret (1981). "Genetic analysis of cytoplasmic ribosomes in fungi." *T. I. B. S.* **6**: 272-274.

- Barreau, C. and J. Bégueret (1982). "DNA - Dependent RNA polymerase III from the fungus Podospora comata. Purification, subunit structure and comparison with the homologous enzyme of a related species." *Eur. J. Biochem.* **129**: 423-428.

- Coppin-Raynal, E. and D. Le Coze (1982). "Mutations relieving hypersensitivity to paromomycin caused by ribosomal suppressors in *Podospora anserina*." *Genet Res Camb* **40**(2): 149-164.

- Coppin, E. (1982). "Ribosomal control of translational fidelity in *Podospora anserina*: a suppressor and an antisuppressor affecting the paromomycin-induced misreading in vitro." *Curr Genet* **5**: 57-63.

- Crouzet, M. and J. Begueret (1982). "Altered ribosomal proteins in emetine resistant strains in the fungus *Podospora anserina*." *Curr Genet* **6**: 39-45.

- Durrens, P. (1982). "*Podospora anserina* mutants defective in cell regeneration and ascospore germination : the presence of a possible lesion in the plasma membrane." *Exp Mycol* **6**: 216-224.

- Durrens, P. and J. Bernet (1982). "*Podospora anserina* mutations inhibiting several developmental alternatives and growth renewal." *Curr Genet* **5**: 181-186.

- Kubicek, R. and G. Lysek (1982). "The morphogenesis of the growth bands in the clock mutant *zonata* of *Podospora anserina*." *Trans. Br. Mycol. Soc.* **79**: 167-170.

- Kuck, U. and K. Esser (1982). "Genetic map of mitochondrial DNA in *Podospora anserina*." *Curr Genet* **5**: 143-147.

- Labarere, J. and M. Bonneu (1982). "Isolation and characterization of plasma membranes from the fungus *Podospora anserina*." *J Bacteriol* **151**(2): 648-656.

- Lazdins, I. B. and D. J. Cummings (1982). "Autonomously replicating sequences in young senescent mitochondrial DNA from *Podospora anserina*." *Curr Genet* **6**: 173-178.

- Lysek, G. and I. D. H. Jennings (1982). "Enhanced K+, Na+ and Mg++ contents in clock mutants of *Podospora anserina* and a role of protons in rhytic mycelial growth." *Physiol. Veg.* **20**: 433-441.

- Picard-Bennoun, M. (1982). "Does translational ambiguity increase during cell differentiation ?" *Fehs Letters* **149**: 167-170.

- Randsholt, N., F. Ibarrondo, et al. (1982). "Analysis of revertants of a ribosomal mutation in *Podospora anserina*: evidence for new ribosomal mutations which confer hypersensitivity to paromomycin." *Biochem Genet* **20**(5-6): 569-584.

- Stahl, U., P. Tudzynski, et al. (1982). "Replication and expression of a bacterial--mitochondrial hybrid plasmid in the fungus *Podospora anserina*." *Proc Natl Acad Sci U S A* **79**(11): 3641-3645.

- Tudzynski, P., U. Stahl, et al. (1982). "Development of a eukaryotic cloning system in *Podospora anserina*. I. Long-lived mutants as potential recipients." *Curr Genet* **6**: 219-222.

- Vierny, C., A. M. Keller, et al. (1982). "A sequence of mitochondrial DNA is associated with the onset of senescence in a fungus." *Nature* **297**(5862): 157-159.

- Wright, R. M., M. A. Horrum, et al. (1982). "Are mitochondrial structural genes selectively amplified during senescence in *Podospora anserina*?" *Cell* **29**(2): 505-515.

- Wright, R. M., J. L. Laping, et al. (1982). "Mitochondrial DNA from *Podospora anserina*. III. Cloning, physical mapping and localization of the robo somal RNA genes." *Molec. Gen. Genet.* **185**: 56-64.

- Bonneu, M. and J. Labarere (1983). "Electrophoretic analysis of plasma membrane proteins of wild-type and differentiation-deficient strains of *Podospora anserina*." *Curr. Microbiol.* **9**: 133-140.

- Crouzet, M. and J. Begueret (1983). "Immunological studies of ribosomal mutants in the fungus *Podospora anserina*." *J Biol Chem* **258**(12): 7618-7622.

- Cummings, D. J. and R. M. Wright (1983). "DNA sequence of the excision sites of a mitochondrial plasmid from senescent *Podospora anserina*." *Nucleic Acids Res* **11**(7): 2111-2119.

- Durrens, P. (1983). "*Podospora anserina* mutants defective in glucose-dependent growth control." *Journal of bacteriology* **154**: 702-707.

- Esser, K., U. Kuck, et al. (1983). "Cloning vectors of mitochondrial origin for eukaryotes, a new concept in genetic engineering." *Curr Genet* **7**: 239-243.

- Fox, T. D. (1983). "Mitochondrial genes in the nucleus." *Nature* **301**: 371.
- Osiewacz, H. D. and K. Esser (1983). "DNA sequence analysis of the mitochondrial plasmid of *Podospora anserina*." *Curr Genet* **7**: 219-233.

- Vilamitjana, J., T. Baltz, et al. (1983). "Probing eukaryotic RNA polymerases B with monoclonal antibodies." *FEBS Lett* **158**(2): 343-348.

- Wright, R. M. and D. J. Cummings (1983). "Integration of mitochondrial gene sequence within the nuclear genome during senescence in a fungus." *Nature* **302**: 86-88.

- Wright, R. M. and D. J. Cummings (1983). "Mitochondrial DNA from *Podospora anserina*. IV. The large ribosomal RNA gene contains two long intervening sequences." *Curr Genet* **7**: 151-157.

- Wright, R. M. and D. J. Cummings (1983). "Transcription of a mitochondrial plasmid during senescence in *Podospora anserina*." *Curr Genet* **7**: 457-464.

- Begueret, J., V. Razanamparany, et al. (1984). "Cloning gene *ura5* for the orotidylic acid pyrophosphorylase of the filamentous fungus *Podospora anserina*: transformation of protoplasts." *Gene* **32**(3): 487-492.

- Bollag, J. M. and A. Leonowicz (1984). "Comparative studies of extracellular fungal laccases." *Appl Environ Microbiol* **48**(4): 849-854.

- Cummings, D. J. (1984). "Mitochondrial DNA in *Podospora anserina*. A molecular approach to cellular senescence." *Monogr Dev Biol* **17**: 254-266.

- Dequard, M. and E. Coppin (1984). "Increase of translational fidelity blocks sporulation in the fungus *Podospora anserina*." *Mol. Gen. Genet.* **195**: 294-299.

- Durrens, P. (1984). "*Podospora anserina* mutation reducing cell survival under glucose starvation." *Exp. Mycol.* **8**: 342-348.

- Jamet-Vierny, C., O. Begel, et al. (1984). "A 20 X 10(3)-base mosaic gene identified on the mitochondrial chromosome of *Podospora anserina*." *Eur J Biochem* **143**(2): 389-394.

- Koll, F., O. Begel, et al. (1984). "Ethidium bromide rejuvenation of sensecent cultures of *Podospora anserina*: Loss of sensecence specific DNA and recovery of normal mitochondrial DNA." *Curr Genet* **8**: 127-134.

- Le Goff, V. and J. Begueret (1984). "Immunological comparison of individual ribosomal proteins in six species of the genus *Podospora*." *Mol Gen Genet* **193**(1): 143-148.

- Le Goff, V., M. Perrot, et al. (1984). "Electrophoretical and immunological comparison of the ribosomal proteins of the fungus *Podospora anserina* and the yeast *Saccharomyces cerevisiae*." *Curr Genet* **9**: 53-58.

- Osiewacz, H. D. and K. Esser (1984). "The mitochondrial plasmid of *Podospora anserina*: a mobile intron of a mitochondrial gene." *Curr Genet* **8**: 299-305.

- Brygoo, Y. and R. Debuchy (1985). "Transformation by integration in *Podospora anserina* I. Methodology and phenomenology." *Mol. Gen. Genet.* **200**: 128-131.

- Cummings, D. J., I. A. MacNeil, et al. (1985). "Excision-amplification of mitochondrial DNA during senescence in *Podospora anserina*. DNA sequence analysis of three unique "plasmids"." *J Mol Biol* **185**(4): 659-680.

- Debuchy, R. and Y. Brygoo (1985). "Cloning of opal suppressor tRNA genes of a filamentous fungus reveals two tRNAserUGA genes with unexpected structural differences." *Embo J* **4**(13A): 3553-3556.

- Dequard-Chablat, M. (1985). "Identification of the structural gene for the S9 ribosomal protein in the fungus *Podospora anserina*: a new protein involved in the control of translational accuracy." *Mol Gen Genet* **200**(2): 343-345.

- Dequard-Chablat, M. (1985). "Ribosomal suppressors in *Podospora anserina*: evidence for two new loci by means of a new screening procedure." *Genet Res Camb* **45**(1): 9-19.

- Durrens, P. and J. Bernet (1985). "Temporal action of mutations inhibiting the accomplishment of quiescence or disrupting development in the fungus *Podospora anserina*." *Genetics* **109**: 37-47.

- Ferrer, S., D. Ramon, et al. (1985). "Protoplasts from *Podospora anserina*: Isolation, purification and transformation." *Curr. Microbiol.* **12**: 301-306.

- Koll, F., L. Belcour, et al. (1985). "A 1100-bp sequence of mitochondrial DNA is involved in senescence process in *Podospora*: study of senescent and mutant cultures." *Plasmid* **14**(2): 106-117.

- Kuck, U., B. Kappelhoff, et al. (1985). "Despite mtDNA polymorphism the mobile intron (plDNA) of the COI gene is present in ten different races of *Podospora anserina*." *Curr Genet* **10**: 59-67.

- Kuck, U., H. D. Osiewacz, et al. (1985). "The onset of senescence is affected by DNA rearrangements of a discontinuous mitochondrial gene in *Podospora anserina*." *Curr Genet* **9**(5): 373-382.

- Labarere, J. and M. Bonneu (1985). "A new method for the screening of mutations related to protoplasmic incompatibility, differentiation and plasma membrane in the fungus *Podospora anserina*." *Genetics* **111**: 259-271.

- Labat, N., M. Perrot, et al. (1985). "Cloning and characterization of the rDNA repeat unit of *Podospora anserina*." *Mol Gen Genet* **199**(1): 154-157.

- Michel, F. and D. J. Cummings (1985). "Analysis of class I introns in a mitochondrial plasmid associated with senescence of *Podospora anserina* reveals extraordinary resemblance to the Tetrahymena ribosomal intron." *Curr Genet* **10**(1): 69-79.

- Picard, M. (1985). "Introns, protein syntheses and aging." *FEBS Lett* **184**: 1-5.
- Belcour, L., F. Koll, et al. (1986). "Are proteins encoded in mitochondrial introns involved in the process of senescence in the fungus *Podospora anserina*?" *Inserm-Eurage John Libbey Eurotext Ltd.* **147**: 63-71.

- Belcour, L. and C. Vierny (1986). "Variable DNA splicing sites of a mitochondrial intron : relationship to the senescence process in *Podospora*." *Embo J* **5**: 609-614.

- Bernet, J. (1986). "*Podospora* mutations reducing cell survival following nutrient exhaustion." *Curr. Microbiol.* **14**: 133-136.

- Böckelmann, B. and K. Esser (1986). "Plasmids of mitochondrial origin in senescent mycelia of *Podospora curvicolla*." *Curr. Genet.* **10**: 803-810.

- Dequard-Chablat, M. (1986). "Genetics of translational fidelity in *Podospora anserina*: are all the genes involved in this ribosomal function identified?" *Curr Genet* **10**(7): 531-536.

- Dequard-Chablat, M. (1986). "Different alterations of the ribosomal protein S7 lead to opposite effects on translational fidelity of the fungus *Podospora anserina*." *The Journal of Biological Chemistry* **261**: 4117-4121.

- Dequard-Chablat, M., E. Coppin-Raynal, et al. (1986). "At least seven ribosomal proteins are involved in the control of translational accuracy in a eukaryotic organism." *J Mol Biol* **190**(2): 167-175.

- Koll, F. (1986). "Does nuclear integration of mitochondrial sequences occur during senescence in *Podospora*?" *Nature* **324**: 597-599.

- Matsuura, E. T., J. M. Domenico, et al. (1986). "An additional class II intron with homology to reverse transcriptase in rapidly senescing *Podospora anserina*." *Curr Genet* **10**(12): 915-922.

- Razanamparany, V. and J. Begueret (1986). "Positive screening and transformation of ura5 mutants in the fungus *Podospora anserina*: characterization of the transformants." *Curr Genet* **10**(11): 811-817.

- Sainsard-Chanet, A. and O. Begel (1986). "Transformation of yeast and *Podospora*: innuity of senescence-specific DNAs." *Mol. Gen. Genet.* **204**: 443-451.

- Steinhilber, W. and D. J. Cummings (1986). "A DNA polymerase activity with characteristics of a reverse transcriptase in *Podospora anserina*." *Curr Genet* **10**(5): 389-392.

- Karsch, T., U. Kuck, et al. (1987). "Mitochondrial group I introns from the filamentous fungus *Podospora anserina* code for polypeptides related to maturases." *Nucleic Acids Res* **15**(16): 6743-6744.

- Koll, F., O. Begel, et al. (1987). "Insertion of short poly d(A) d(T) sequences at recombination junctions in mitochondrial DNA of *Podospora*." *Mol. Gen. Genet.* **209**: 630-632.

- Perrot, M., C. Barreau, et al. (1987). "Nonintegrative transformation in the filamentous fungus *Podospora anserina*: stabilization of a linear vector by the chromosomal ends of *Tetrahymena thermophila*." *Mol Cell Biol* **7**(5): 1725-1730.

- Picard, M., R. Debuchy, et al. (1987). "Transformation by integration in *Podospora anserina* II. Targeting to the resident locus with cosmids and instability of the transformants." *Mol. Gen. Genet.* **210**: 129-134.

- Schmidt, U., M. Kosack, et al. (1987). "Lariat RNA of a group II intron in a filamentous fungus." *Curr Genet* **12**: 291-295.

- Turcq, B. and J. Begueret (1987). "The ura5 gene of the filamentous fungus *Podospora anserina*: nucleotide sequence and expression in transformed strains." *Gene* **53**: 201-209.

- Turker, M. S. and D. J. Cummings (1987). "*Podospora anserina* does not senesc when serially passaged in liquid culture." *J Bacteriol* **169**(2): 454-460.

- Turker, M. S., J. M. Domenico, et al. (1987). "Excision-amplification of mitochondrial DNA during senescence in *Podospora anserina*. A potential role for an 11 base-pair consensus sequence in the excision process." *J Mol Biol* **198**(2): 171-185.

- Turker, M. S., J. M. Domenico, et al. (1987). "A novel family of mitochondrial plasmids associated with longevity mutants of *Podospora anserina*." *J Biol Chem* **262**(5): 2250-2255.

- Turker, M. S., J. G. Nelson, et al. (1987). "A *Podospora anserina* longevity mutant with a temperature-sensitive phenotype for senescence." *Mol Cell Biol* **7**(9): 3199-3204.

- Vilamitjana, J. and C. Barreau (1987). "A monoclonal antibody directed against a small subunit of RNA polymerase B blocks the initiation step." *Eur. J. Biochem* **162**: 317-323.

- Bernet, J. (1988). "*Podospora* growth control mutations inhibit apical cell anastomosis and protoperithecium formation." *Exp Mycol* **12**(3): 217-222.

- Cummings, D. J. and J. M. Domenico (1988). "Sequence analysis of mitochondrial DNA from *Podospora anserina*. Pervasiveness of a class I intron in three separate genes." *J Mol Biol* **204**(4): 815-839.

- Cummings, D. J., J. M. Domenico, et al. (1988). "DNA sequence and organization of the mitochondrial ND1 gene from *Podospora anserina*: analysis of alternate splice sites." *Curr Genet* **14**(3): 253-264.

- Debuchy, R., E. Coppin-Raynal, et al. (1988). "Chromosome walking towards a centromere in the filamentous fungus *Podospora anserina*: cloning of a sequence lethal at a two-copy state." *Curr Genet* **13**: 105-111.

- Kieu-Ngoc, A. and E. Coppin-Raynal (1988). "Identification of two genes controlling kasugamycin resistance in the filamentous fungus *Podospora anserina*." *Genet Res Camb* **51**(3): 179-184.

- Razanamparany, V. and J. Bégueret (1988). "Non-homologous integration of transforming vectors in the fungus *Podospora anserina*: sequences of junctions at the integration sites." *Gene* **74**(2): 399-409.
- Schulte, E., U. Kück, et al. (1988). "Extrachromosomal mutants from *Podospora anserina*: permanent vegetative growth in spite of multiple recombination events in the mitochondrial genome." *Mol Gen Genet.* **211**: 342-349.

- Vierny-Jamet, C. (1988). "Senescence in *Podospora anserina*: a possible role for nucleic acid interacting proteins suggested by the sequence analysis of a mitochondrial DNA region specifically amplified in senescent cultures." *Gene* **74**(2): 387-398.

- Berges, T. and C. Barreau (1989). "Heat shock at an elevated temperature improves transformation efficiency of protoplasts from *Podospora anserina*." *J Gen Microbiol* **135*(Pt 3): 601-604.

- Coppin-Raynal, E., M. Picard, et al. (1989). "Transformation by integration in *Podospora anserina*. III. Replacement of a chromosome segment by a two-step process." *Mol Gen Genet* **219**(1-2): 270-276.

- Cummings, D. J., J. M. Domenico, et al. (1989). "DNA sequence and secondary structures of the large subunit rRNA coding regions and its two class I introns of mitochondrial DNA from *Podospora anserina*." *J Mol Evol* **28**(3): 242-255.

- Cummings, D. J., J. M. Domenico, et al. (1989). "DNA sequence, structure, and phylogenetic relationship of the small subunit rRNA coding region of mitochondrial DNA from *Podospora anserina*." *J Mol Evol* **28**(3): 232-241.

- Cummings, D. J., F. Michel, et al. (1989). "DNA sequence analysis of the 24.5 kilobase pair cytochrome oxidase subunit I mitochondrial gene from *Podospora anserina*: a gene with sixteen introns." *Curr Genet* **16**(5-6): 381-406.

- Cummings, D. J., F. Michel, et al. (1989). "DNA sequence analysis of the apocytochrome b gene of *Podospora anserina*: a new family of intronic open reading frame." *Curr Genet* **16**(5-6): 407-418.

- Fernadez-Larrea, J. and U. Stahl (1989). "Transformation of *Podospora anserina* with a dominant resistance gene." *Curr. Genet.* **16**: 57-60.

- Fincham, J. R. (1989). "Transformation in fungi." *Microbiol Rev* **53**(1): 148-170.

- Koll, F. and L. Belcour (1989). "Are intron-encoded specific endonucleases responsible for nonhomologous recombination ?" *Trends Genet* **5**: 173.

- Krug, J. C. and R. S. Khan (1989). "New records and new species of *Podospora* from East Africa." *Canadian Journal of Botany* **67**(4): 1174-1182.

- Kück, H.-U. (1989). "Mitochondrial DNA rearrangements in *Podospora anserina*." *Exp Mycol* **13**: 111-120.

- Osiewacz, H. D., J. Hermanns, et al. (1989). "Mitochondrial DNA rearrangements are correlated with a delayed amplification of the mobile intron (pI DNA) in a long-lived mutant of *Podospora anserina*." *Mutat Res* **219**(1): 9-15.

- Schulte, E., U. Kück, et al. (1989). "Multipartite structure of mitochondrial DNA in a fungal longlife mutant." *Plasmid* **21**(1): 79-84.

- Cummings, D. J. and J. M. Domenico (1990). "Mitochondrial DNA from *Podospora anserina*: transformation to senescence via projectile injection of plasmids." *Molecular biology of aging*: 91-101.

- Cummings, D. J., K. L. McNally, et al. (1990). "The complete DNA sequence of the mitochondrial genome of *Podospora anserina*." *Curr Genet* **17**(5): 375-402.

- Cummings, D. J., F. Michel, et al. (1990). "Mitochondrial DNA sequence analysis of the cytochrome oxidase subunit II gene from *Podospora anserina*. A group IA intron with a putative alternative splice site." *J Mol Biol* **212**(2): 287-294.

- Cummings, D. J., F. Michel, et al. (1990). "DNA sequence analysis of the mitochondrial *ND4L-ND5* gene complex from *Podospora anserina*. Duplication of the *ND4L* gene within its intron." *J Mol Biol* **212**(2): 269-286.

- Deleu, C., B. Turcq, et al. (1990). "repa, a repetitive and dispersed DNA sequence of the filamentous fungus *Podospora anserina*." *Nucleic Acids Res* **18**(16): 4901-4903.

- Lysek, G., H. Hohmeyer, et al. (1990). "A spontaneous benomyl-resistant mutant of *Podospora anserina* exhibiting a diurnal growth rhythm." *Cellular and Molecular Life Sciences CMLS* **46**: 517-520.

- Osiewacz, H. D. (1990). "Molecular analysis of aging processes in fungi." *Mutat Res* **237**: 1-8.

- Osiewacz, H. D., A. Clairmont, et al. (1990). "Electrophoretic karyotype of the ascomycete *Podospora anserina*." *Curr. Genet.* **18**: 481-483.

- Sainsard-Chanet, A. and O. Begel (1990). "Insertion of an LrDNA gene fragment and of filler DNA at a mitochondrial exon-intron junction in *Podospora*." *Nucleic Acids Res* **18**(4): 779-783.

- Schmidt, U., B. Riederer, et al. (1990). "Self-splicing of the mobile group II intron of the filamentous fungus *Podospora anserina* (COI I1) *in vitro*." *EMBO J* **9**(7): 2289-2298.

- Sellem, C. H., A. Sainsard-Chanet, et al. (1990). "Detection of a protein encoded by a class II mitochondrial intron of *Podospora anserina*." *Mol Gen Genet* **224**(2): 232-240.

- Silliker, M. E. and D. J. Cummings (1990). "A mitochondrial DNA rearrangement and three new mitochondrial plasmids from long-lived strains of *Podospora anserina*." *Plasmid* **24**(1): 37-44.

- Silliker, M. E. and D. J. Cummings (1990). "Genetic and molecular analysis of a long-lived strain of *Podospora anserina*." *Genetics* **125**(4): 775-781.

- Turcq, B., M. Denayrolles, et al. (1990). "Isolation of two allelic incompatibility genes s and S of the fungus *Podospora anserina*." *Curr Genet* **17**: 297-303.

- Belcour, L., O. Begel, et al. (1991). "A site-specific deletion in mitochondrial DNA of *Podospora* is under the control of nuclear genes." *Proc Natl Acad Sci U S A* **88**(9): 3579-3583.
- Belcour, L., M. Dequard-Chablat, et al. (1991). "Délétion site-spécifique de l'ADN mitochondrial sous le contrôle de deux gènes nucléaires." *Médecine/Sciences* **7**: 628-629.

- Bernet, J. (1991). "Aerial organs and cell death in *Podospora anserina* mutants: relationship with protoplasmic incompatibility." *Exp Mycol* **15**(3): 215-222.

- Dequard-Chablat, M. (1991). "Translation, oncogenesis and myopathies." *Trends Genet* **7**(8): 240-241.

- Osiewacz, H. D., A. Skaletz, et al. (1991). "Integrative transformation of the ascomycete *Podospora anserina*: identification of the mating-type locus on chromosome VII of electrophoretically separated chromosomes." *Appl Microbiol Biotechnol* **35**(1): 38-45.

- Picard, M., R. Debuchy, et al. (1991). "Cloning the mating types of the heterothallic fungus *Podospora anserina*: developmental features of haploid transformants carrying both mating types." *Genetics* **128*(3): 539-547.

- Ridder, R., K. P. Künkele, et al. (1991). "Sequence of the nuclear ATP synthase subunit 9 gene of *Podospora anserina*: lack of similarity to the mitochondrial genome." *Curr Genet* **20**(4): 349-351.

- Turcq, B., C. Deleu, et al. (1991). "Two allelic genes responsible for vegetative incompatibility in the fungus *Podospora anserina* are not essential for cell viability." *Mol Gen Genet* **228**(1-2): 265-269.

- Bellemère, A., M. C. Janex-Favre, et al. (1992). "Diversité ultrastructurale de la paroi ascosporale chez quelques eupyrénomycètes." *Cryptogamie, Mycol.* **13**: 215-246.

- Bernet, J. (1992). "In *Podospora anserina*, protoplasmic incompatibility genes are involved in cell death control via multiple gene interactions." *Heredity* **68**: 79-87.

- Bernet, J. (1992). "A gene suppressing the allelic protoplasmic incompatibility specified by genes at five different loci in *Podospora anserina*." *J Gen Microbiol* **138**: 2567-2574.

- Debuchy, R. and E. Coppin (1992). "The mating types of *Podospora anserina*: functional analysis and sequence of the fertilization domains." *Mol Gen Genet* **233**(1-2): 113-121.

- Frese, D. and U. Stahl (1992). "Oxidative stress and ageing in the fungus *Podospora anserina*." *Mech Ageing Dev* **65**(2-3): 277-288.

- Griffiths, A. J. F. (1992). "Fungal senescence." *Annu. Rev. Genet.* **26**: 351-372.

- Hermanns, J. and H. D. Osiewacz (1992). "The linear mitochondrial plasmid pAL2-1 of a long-lived *Podospora anserina* mutant is an inverteron encoding a DNA and RNA polymerase." *Curr Genet* **22**(6): 491-500.

- Kämper, U., U. Kück, et al. (1992). "The mitochondrial tyrosyl-tRNA synthetase of *Podospora anserina* is a bifunctional enzyme active in protein synthesis and RNA splicing." *Mol Cell Biol* **12**(2): 499-511.

- Kempken, F., J. Hermanns, et al. (1992). "Evolution of linear plasmids." *J Mol Evol* **35**(6): 502-513.

- Nauta, M. J. and R. F. Hoekstra (1992). "Evolution of reproductive systems in filamentous ascomycetes. II. Evolution of hermaphroditism and other reproductive strategies." *Heredity* **68**: 537-546.

- Nauta, M. J. and R. F. Hoekstra (1992). "Evolution of reproductive systems in filamentous ascomycetes. I. Evolution of mating types." *Heredity* **68**: 405-410.

- Osiewacz, H. D. and J. Hermanns (1992). "The role of mitochondrial DNA rearrangements in aging and human diseases." *Aging Clin. Exp. Res.* **4**: 273-286.

- Ridder, R. and H. D. Osiewacz (1992). "Sequence analysis of the gene coding for glyceraldehyde-3-phosphate dehydrogenase (gpd) of *Podospora anserina*: use of homologous regulatory sequences to improve transformation efficiency." *Curr Genet* **21**(3): 207-213.

- Schmidt, U., E. Budde, et al. (1992). "Self-splicing of a mitochondrial group I intron from the cytochrome b gene of the ascomycete *Podospora anserina*." *Mol Gen Genet* **233**(1-2): 71-80.

- Arnaise, S., D. Zickler, et al. (1993). "Heterologous expression of mating-type genes in filamentous fungi." *Proc Natl Acad Sci U S A* **90**(14): 6616-6620.

- Coppin, E., S. Arnaise, et al. (1993). "Deletion of the mating-type sequences in *Podospora anserina* abolishes mating without affecting vegetative functions and sexual differentiation." *Mol Gen Genet* **241**(3-4): 409-414.

- Debuchy, R., S. Arnaise, et al. (1993). "The *mat*- allele of *Podospora anserina* contains three regulatory genes required for the development of fertilized female organs." *Mol Gen Genet* **241**(5-6): 667-673.

- Deleu, C., C. Clavé, et al. (1993). "A single amino acid difference is sufficient to elicit vegetative incompatibility in the fungus *Podospora anserina*." *Genetics* **135**(1): 45-52.

- Javerzat, J. P., V. Bhattachjerjee, et al. (1993). "Isolation of telomeric DNA from the filamentous fungus *Podospora anserina* and construction of a self-replicating linear plasmid showing high transformation frequency." *Nucleic Acids Res* **21**(3): 497-504.

- Javerzat, J. P., C. Jacquier, et al. (1993). "Assignment of linkage groups to the electrophoretically-separated chromosomes of the fungus *Podospora anserina*." *Curr Genet* **24**(3): 219-222.

- Nauta, M. J. and R. F. Hoekstra (1993). "Evolutionary dynamics of spore killers." *Genetics* **135**(3): 923-930.

- Nauta, M. J., M. van der Gaag, et al. (1993). "A spore killer in a new isolate of *Podospora anserina*." *Fungal Genet. Newsl.* **40A**: 36.

- Sainsard-Chanet, A., O. Begel, et al. (1993). "DNA deletion of mitochondrial introns is correlated with the process of senescence in *Podospora anserina*." *J Mol Biol* **234**(1): 1-7.

- Schmidt, U., R. Sägebarth, et al. (1993). "Self-splicing of a *Podospora anserina* group IIA intron *in vitro*. Effects of 3'-terminal intron alterations on cleavage at the 5' and 3' splice site." *J Mol Biol* **231**(3): 559-568.
- Sellem, C. H., G. Lecellier, et al. (1993). "Transposition of a group II intron." *Nature* **366**(6451): 176-178.

- Begueret, J., B. Turcq, et al. (1994). "Vegetative incompatibility in filamentous fungi: het genes begin to talk." *Trends Genet* **10**: 441-446.

- Belcour, L., A. Sainsard-Chanet, et al. (1994). "Mobile group II introns, DNA circles, reverse transcriptase and senescence (Group II introns, transposition, aging, mitochondria, fungi)." *Genetica* **93**: 225-228.

- Dequard-Chablat, M. and C. H. Sellem (1994). "The S12 ribosomal protein of *Podospora anserina* belongs to the S19 bacterial family and controls the mitochondrial genome integrity through cytoplasmic translation." *J Biol Chem* **269**(21): 14951-14956.

- Fassbender, S., K. H. Bruhl, et al. (1994). "Reverse transcriptase activity of an intron encoded polypeptide." *EMBO J* **13**(9): 2075-2083.

- Hermanns, J., A. Asseburg, et al. (1994). "Evidence for a life span-prolonging effect of a linear plasmid in a longevity mutant of *Podospora anserina*." *Mol Gen Genet* **243**(3): 297-307.

- Hermanns, J. and H. D. Osiewacz (1994). "Three mitochondrial unassigned open reading frames of *Podospora anserina* represent remnants of a viral-type RNA polymerase gene." *Curr Genet* **25**(2): 150-157.

- Hoekstra, R. F. (1994). "Population genetics of filamentous fungi." *Antonie Van Leeuwenhoek* **65**(3): 199-204.

- Jamet-Vierny, C. and E. Shechter (1994). "Senescence-specific mitochondrial DNA molecules in *P. anserina*: evidence for transcription and normal processing of the RNA." *Curr Genet* **25**(6): 538-544.

- Knoop, V., S. Kloska, et al. (1994). "On the identification of group II introns in nucleotide sequence data." *J Mol Biol* **242**(4): 389-396.

- Lecellier, G. and P. Silar (1994). "Rapid methods for nucleic acids extraction from Petri dish grown mycelia." *Current Genetics* **25**: 122-123.

- Marbach, K., J. Fernandez-Larrea, et al. (1994). "Reversion of a long-living, undifferentiated mutant of *Podospora anserina* by copper." *Curr Genet* **26**(2): 184-186.

- Nauta, M. J. and R. F. Hoekstra (1994). "Evolution of vegetative incompatibility in filamentous Ascomycetes. I. Deterministic models." *Evolution* **48**(4): 979-995.

- Osiewacz, H. D. (1994). "A versatile shuttle cosmid vector for the efficient construction of genomic libraries and for the cloning of fungal genes." *Curr Genet* **26**(1): 87-90.

- Osiewacz, H. D. (1994). "Biologisches Altern und mitochondriale DNA-Instabilitäten." *Bioscope* **2**: 21-28.

- Raju, N. B. (1994). "Ascomycete Spore killers: Chromosomal elements that distort genetic ratios among the products of meiosis." *Mycologia* **86**(4): 461-473.

- Raju, N. B. and D. D. Perkins (1994). "Divers programs of ascus development in pseudohomothallic species of *Neurospora*, *Gelasinospora*, and *Podospora*." *Dev Genet* **15**(1): 104-118.

- Sainsard-Chanet, A., O. Begel, et al. (1994). "DNA double-strand break in vivo at the 3' extremity of exons located upstream of group II introns. Senescence and circular DNA introns in *Podospora mitochondria*." *J Mol Biol* **242**(5): 630-643.

- Sainsard-Chanet, A., C. Sellem, et al. (1994). "Sénescence chez les champignons filamenteurs." *Médecine/Sciences* **5**(10): 574-576.

- Saupe, S., C. Descamps, et al. (1994). "Inactivation of the *Podospora anserina* vegetative incompatibility locus het-c, whose product resembles a glycolipid transfer protein, drastically impairs ascospore production." *Proc Natl Acad Sci U S A* **91**(13): 5927-5931.

- Sellem, C. H. and L. Belcour (1994). "The *in vivo* use of alternate 3'-splice sites in group I introns." *Nucleic Acids Res* **22**(7): 1135-1137.

- Silar, P. (1994). "Is translational accuracy an out-dated topic?" *Trends Genet* **10**(3): 71-72.

- Silar, P. and M. Picard (1994). "Increased longevity of EF-1 alpha high-fidelity mutants in *Podospora anserina*." *J Mol Biol* **235**(1): 231-236.

- Thompson-Coffe, C. and D. Zickler (1994). "How the cytoskeleton recognizes and sorts nuclei of opposite mating type during the sexual cycle in filamentous ascomycetes." *Dev Biol* **165**(1): 257-271.

- Berteaux-Lecellier, V., M. Picard, et al. (1995). "A nonmammalian homolog of the *PAF1* gene (Zellweger syndrome) discovered as a gene involved in caryogamy in the fungus *Podospora anserina*." *Cell* **81**(7): 1043-1051.

- Hermanns, J., A. Asseburg, et al. (1995). "Evidence for giant linear plasmids in the ascomycete *Podospora anserina*." *Curr Genet* **27**(4): 379-386.

- Hermanns, J., F. Debets, et al. (1995). "A novel family of linear plasmids with homology to plasmid pAL2-1 of *Podospora anserina*." *Mol Gen Genet* **246**(5): 638-647.

- Hur, M. and R. B. Waring (1995). "Two group I introns with a C.G basepair at the 5' splice-site instead of the very highly conserved U.G basepair: is selection post-translational?" *Nucleic Acids Res* **23**(21): 4466-4470.

- Kempken, F. (1995). "Horizontal transfer of a mitochondrial plasmid." *Mol Gen Genet* **248**(1): 89-94.

- Saupe, S., B. Turcq, et al. (1995). "Sequence diversity and unusual variability at the het-c locus involved in vegetative incompatibility in the fungus *Podospora anserina*." *Curr Genet* **27**(5): 466-471.

- Saupe, S., B. Turcq, et al. (1995). "A gene responsible for vegetative incompatibility in the fungus *Podospora anserina* encodes a protein with a GTP-binding motif and G beta homologous domain." *Gene* **162**(1): 135-139.
- Silar, P. (1995). "Two new easy-to-use vectors for transformations." *Fungal Genetic Newsletter* **42**: 73.

- Zickler, D., S. Arnaise, et al. (1995). "Altered mating-type identity in the fungus *Podospora anserina* leads to selfish nuclei, uniparental progeny, and haploid meiosis." *Genetics* **140**(2): 493-503.

- Contamine, V., G. Lecellier, et al. (1996). "Premature death in *Podospora anserina*: sporadic accumulation of the deleted mitochondrial genome, translational parameters and innocuity of the mating types." *Genetics* **144**(2): 541-555.

- Fernandez-Larrea, J. and U. Stahl (1996). "Isolation and characterization of a laccase gene from *Podospora anserina*." *Mol Gen Genet* **252**(5): 539-551.

- Hermanns, J. and H. D. Osiewacz (1996). "Induction of longevity by cytoplasmic transfer of a linear plasmid in *Podospora anserina*." *Curr Genet* **29**(3): 250-256.

- Koll, F., J. Boulay, et al. (1996). "Contribution of ultra-short invasive elements to the evolution of the mitochondrial genome in the genus *Podospora*." *Nucleic Acids Research* **24**(9): 1734-1741.

- Loubradou, G., J. Bégueret, et al. (1996). "An additional copy of the adenylate cyclase-encoding gene relieves developmental defects produced by a mutation in a vegetative incompatibility-controlling gene in *Podospora anserina*." *Gene* **170**(1): 119-123.

- Nauta, M. J. and R. F. Hoekstra (1996). "Vegetative incompatibility in Ascomycetes: highly polymorphic but selectively neutral?" *J Theor Biol* **183**(1): 67-76.

- Osiewacz, H. D., A. Hamann, et al. (1996). "Genome analysis of filamentous fungi: identification of a highly conserved simple repetitive sequence in different strains of *Podospora anserina*." *Microbiol Res* **151**: 1-8.

- Osiewacz, H. D. and U. Nuber (1996). "GRISEA, a putative copper-activated transcription factor from *Podospora anserina* involved in differentiation and senescence." *Mol Gen Genet* **252**(1-2): 115-124.

- Pöggeler, S., C. Schwerk, et al. (1996). "Efficient synthesis of a 72-kDa mitochondrial polypeptide using the yeast Ty expression system." *Biochem Biophys Res Commun* **219**(3): 890-899.

- Rossignol, M. and P. Silar (1996). "Genes that control longevity in *Podospora anserina*." *Mech Ageing Dev* **90**(3): 183-193.

- Schwartz, T. and H. D. Osiewacz (1996). "Telomere length does not change during senescence of the ascomycete *Podospora anserina*." *Mutat Res* **316**(5-6): 193-199.

- Sellem, C. H., Y. d'Aubenton-Carafa, et al. (1996). "Mitochondrial intronic open reading frames in *Podospora* : mobility and consecutive exonic sequence variations." *Genetics* **143**: 777-778.

- Silliker, M. E., M. R. Liotta, et al. (1996). "Elimination of mitochondrial mutations by sexual reproduction: two *Podospora anserina* mitochondrial mutants yield only wild-type progeny when mated." *Curr Genet* **30**(4): 318-324.

- Arnaise, S., R. Debuchy, et al. (1997). "What is a bona fide mating-type gene? Internuclear complementation of *mat* mutants in *Podospora anserina*." *Mol Gen Genet* **256**(2): 169-178.

- Belcour, L., M. Rossignol, et al. (1997). "Plasticity of the mitochondrial genome in *Podospora*. Polymorphism for 15 optional sequences: group-I, group-II introns, intronic ORFs and an intergenic region." *Current Genetics* **31**(4): 308-317.

- Borghouts, C., E. Kimpel, et al. (1997). "Mitochondrial DNA rearrangements of *Podospora anserina* are under the control of the nuclear gene *grisea*." *Proc Natl Acad Sci U S A* **94**(20): 10768-10773.

- Coppin, E., R. Debuchy, et al. (1997). "Mating types and sexual development in filamentous ascomycetes." *Microbiol Mol Biol Rev* **61**(4): 411-428.

- Coustou, V., C. Deleu, et al. (1997). "The protein product of the *het-s* heterokaryon incompatibility gene of the fungus *Podospora anserina* behaves as a prion analog." *Proc Natl Acad Sci U S A* **94**(18): 9773-9778.

- Dequard-Chablat, M. and A. Rötig (1997). "Homologous and heterologous expression of a ribosomal protein gene in *Podospora anserina* requires an intron." *Mol Gen Genet* **253**(5): 546-552.

- Espagne, E., P. Balhadere, et al. (1997). "Reactivity in vegetative incompatibility of the HET-E protein of the fungus *Podospora anserina* is dependent on GTP-binding activity and a WD40 repeated domain." *Mol Gen Genet* **256**(6): 620-627.

- Gagny, B., M. Rossignol, et al. (1997). "Cloning, sequencing, and transgenic expression of *Podospora curvicolla* and *Sordaria macrospora* eEF1A genes: relationship between cytosolic translation and longevity in filamentous fungi." *Fungal Genet Biol* **22**(3): 191-198.

- Hur, M., W. J. Geese, et al. (1997). "Self-splicing activity of the mitochondrial group-I introns from *Aspergillus nidulans* and related introns from other species." *Curr Genet* **32**(6): 399-407.

- Jamet-Vierny, C., J. Boulay, et al. (1997). "Contribution of various classes of defective mitochondrial DNA molecules to senescence in *Podospora anserina*." *Curr Genet* **31**(2): 171-178.

- Jamet-Vierny, C., J. Boulay, et al. (1997). "Intramolecular cross-overs generate deleted mitochondrial DNA molecules in *Podospora anserina*." *Curr Genet* **31**(2): 162-170.

- Jamet-Vierny, C., V. Contamine, et al. (1997). "Mutations in genes encoding the mitochondrial outer membrane proteins Tom70 and Mdm10 of *Podospora anserina* modify the spectrum of mitochondrial DNA rearrangements associated with cellular death." *Mol Cell Biol* **17**(11): 6359-6366.

- Loubradou, G., J. Bégueret, et al. (1997). "A mutation in an *HSP90* gene affects the sexual cycle and suppresses vegetative incompatibility in the fungus *Podospora anserina*." *Genetics* **147**(2): 581-588.
- Osiewacz, H. D. (1997). "Genetic regulation of aging." *J Mol Med* **75**(10): 715-727.

- Osiewacz, H. D. and A. Hamann (1997). "DNA reorganization and biological aging." *A review Biochemistry (Moscow)* **62**: 1275-1248.

- Pöggeler, S., S. Risch, et al. (1997). "Mating-type genes from the homothallic fungus *Sordaria macrospora* are functionally expressed in a heterothallic ascomycete." *Genetics* **147**(2): 567-580.

- Sellem, C. H. and L. Belcour (1997). "Intron open reading frames as mobile elements and evolution of a group I intron." *Mol. Biol. Evol.* **14**: 518-526.

- Silar, P., F. Koll, et al. (1997). "Cytosolic ribosomal mutations that abolish accumulation of circular intron in the mitochondria without preventing senescence of *Podospora anserina*." *Genetics* **145**(3): 697-705.

- Silar, P., C. Vierny, et al. (1997). "Génétique de deux dégénérances cellulaires chez le champignon filamenteux *Podospora anserina*." *C. R. Soc. Biol. Paris* **191**: 563-577.

- Siliker, M. E., J. A. Monroe, et al. (1997). "Evaluation of the efficiency of sexual reproduction in restoring *Podospora anserina* mitochondrial DNA to wild-type." *Curr Genet* **32**(4): 281-286.

- Wang, H., K. B. Gloer, et al. (1997). "Anserinones A and B: new antifungal and antibacterial benzoquinones from the coprophilous fungus *Podospora anserina*." *J Nat Prod* **60**(6): 629-631.

- Wickner, R. B. (1997). "A new prion controls fungal cell fusion incompatibility." *Proc Natl Acad Sci U S A* **94**(19): 10012-10014.

- Barreau, C., M. Iskandar, et al. (1998). "The mod-A suppressor of nonallelic heterokaryon incompatibility in *Podospora anserina* encodes a proline-rich polypeptide involved in female organ formation." *Genetics* **149**(2): 915-926.

- Barreau, C., M. Iskandar, et al. (1998). "Use of a linear plasmid containing telomeres as an efficient vector for direct cloning in the filamentous fungus *Podospora anserina*." *Fungal Genet Biol* **25**(1): 22-30.

- Berteaux-Lecellier, V., D. Zickler, et al. (1998). "A homologue of the yeast *SHE4* gene is essential for the transition between the syncytial and cellular stages during sexual reproduction of the fungus *Podospora anserina*." *EMBO J* **17**(5): 1248-1258.

- Borghouts, C. and H. D. Osiewacz (1998). "GRISEA, a copper-modulated transcription factor from *Podospora anserina* involved in senescence and morphogenesis, is an ortholog of MAC1 in *Saccharomyces cerevisiae*." *Mol Gen Genet* **260**(5): 492-502.

- Bourges, N., A. Groppi, et al. (1998). "Regulation of gene expression during the vegetative incompatibility reaction in *Podospora anserina*. Characterization of three induced genes." *Genetics* **150**(2): 633-641.

- Caretta, G., E. Piontelli, et al. (1998). "Some coprophilous fungi from Kenya." *Mycopathologia* **142**(3): 125-134.

- Contamine, V. and M. Picard (1998). "Escape from Premature Death Due to Nuclear Mutations in *Podospora anserina*: Repeal versus Respite." *Fungal Genet Biol* **23**(3): 223-236.

- Gagny, B. and P. Silar (1998). "Identification of the genes encoding the cytosolic translation release factors from *Podospora anserina* and analysis of their role during the life cycle." *Genetics* **149**(4): 1763-1775.

- Hamann, A. and H. D. Osiewacz (1998). "Genome analysis of filamentous fungi: identification and characterization of an unusual GT-rich minisatellite in the ascomycete *Podospora anserina*." *Curr Genet* **34**(2): 88-92.

- Paoletti, M., C. Clavé, et al. (1998). "Characterization of a gene from the filamentous fungus *Podospora anserina* encoding an aspartyl protease induced upon carbon starvation." *Gene* **210**(1): 45-52.

- Sainsard-Chanet, A., O. Begel, et al. (1998). "Two co-existing mechanisms account for the large-scale deletions of mitochondrial DNA in *Podospora anserina* that involve the 5' border of a group-II intron." *Curr Genet* **34**(4): 326-335.

- Salvo, J. L., B. Rodeghier, et al. (1998). "Optional introns in mitochondrial DNA of *Podospora anserina* are the primary source of observed size polymorphisms." *Fungal Genet Biol* **23**(2): 162-168.

- Turcq, B. and J. Bégueret (1998). "L'incompatibilité végétative chez les champignons filamenteux : quelles informations apporte la caractérisation des gènes impliqués." *S.F.G.* **14**: 6-7.

- van der Gaag, M., A. J. M. Debets, et al. (1998). "The dynamics of pAL2-1 homologous linear plasmids in *Podospora anserina*." *Mol Gen Genet* **258**(5): 521-529.

- Begel, O., J. Boulay, et al. (1999). "Mitochondrial group II introns, cytochrome c oxidase, and senescence in *Podospora anserina*." *Mol Cell Biol* **19**(6): 4093-4100.

- Coustou, V., C. Deleu, et al. (1999). "Mutational analysis of the [Het-s] prion analog of *Podospora anserina*. A short N-terminal peptide allows prion propagation." *Genetics* **153**(4): 1629-1640.

- Debuchy, R. (1999). "Internuclear recognition: A possible connection between euascomycetes and homobasiomycetes." *Fungal Genet Biol* **27**(2-3): 218-223.

- Hurst, L. D. (1999). "The evolution of genomic anatomy." *Trends Ecol Evol* **14**(3): 108-112.

- Jamet-Vierny, C., M. Rossignol, et al. (1999). "What triggers senescence in *Podospora anserina*?" *Fungal Genet Biol* **27**(1): 26-35.

- Khashnobish, A., A. Hamann, et al. (1999). "Modulation of gene expression by (CA)n microsatellites in the filamentous ascomycete *Podospora anserina*." *Appl Microbiol Biotechnol* **52**(2): 191-195.

- Kimpel, E. and H. D. Osiewacz (1999). "PaGrg1, a glucose-repressible gene of *Podospora anserina* that is differentially expressed during lifespan." *Curr Genet* **35**(5): 557-563.
- Loubradou, G., J. Bégueret, et al. (1999). "MOD-D, a Galpha subunit of the fungus *Podospora anserina*, is involved in both regulation of development and vegetative incompatibility." *Genetics* **152**(2): 519-528.

- Osiewacz, H. D. and E. Kimpel (1999). "Mitochondrial-nuclear interactions and lifespan control in fungi." *Exp Gerontol* **34**(8): 901-909.

- Silar, P. and M. J. Daboussi (1999). "Non-conventional infectious elements in filamentous fungi." *Trends Genetics* **15**(4): 141-145.

- Silar, P., V. Haedens, et al. (1999). "Propagation of a novel cytoplasmic, infectious and deleterious determinant is controlled by translational accuracy in *Podospora anserina*." *Genetics* **151**(1): 87-95.

- Ter-Avanesyan, M. D. and V. V. Kushnirov (1999). "Prions: infectious proteins with genetic properties." *Biochemistry (Mosc)* **64**(12): 1382-1390.

- Thompson-Coffe, C., G. Borioli, et al. (1999). "Pyruvate decarboxylase filaments are associated with the cortical cytoskeleton of asci and spores over the sexual cycle of filamentous ascomycetes." *Fungal Genet Biol* **26**(1): 71-80.

- Wickner, R. B., K. L. Taylor, et al. (1999). "Prions in *Saccharomyces* and *Podospora spp.*: protein-based inheritance." *Microbiol Mol Biol Rev* **63**(4): 844-861.

- Averbeck, N. B., O. N. Jensen, et al. (2000). "Identification and characterization of PaMTH1, a putative O-methyltransferase accumulating during senescence of *Podospora anserina* cultures." *Curr Genet* **37**(3): 200-208.

- Borghouts, C., S. Kerschner, et al. (2000). "Copper-dependence of mitochondrial DNA rearrangements in *Podospora anserina*." *Curr Genet* **37**(4): 268-275.

- Borghouts, C. and H. D. Osiewacz (2000). "Nuclear-mitochondrial interactions involved in aging in *Podospora anserina*." *Ann N Y Acad Sci* **908**: 291-294.

- Contamine, V. and M. Picard (2000). "Maintenance and integrity of the mitochondrial genome : a plethora of nuclear genes in the budding yeast." *Mol Microbiol*, **64**: 281-315.

- Coppin, E. and R. Debuchy (2000). "Co-expression of the mating-type genes involved in internuclear recognition is lethal in *Podospora anserina*." *Genetics* **155**(2): 657-669.

- Dufour, E., J. Boulay, et al. (2000). "A causal link between respiration and senescence in *Podospora anserina*." *Proc Natl Acad Sci U S A* **97**(8): 4138-4143.

- Graïa, F., V. Berteaux-Lecellier, et al. (2000). "ami1, an orthologue of the *Aspergillus nidulans* apsA gene, is involved in nuclear migration events throughout the life cycle of *Podospora anserina*." *Genetics* **155**(2): 633-646.

- Hamann, A., F. Feller, et al. (2000). "The degenerate DNA transposon Pat and repeat-induced point mutation (RIP) in *Podospora anserina*." *Mol Gen Genet* **263**(6): 1061-1069.

- Hamann, A., F. Feller, et al. (2000). "Yeti-a degenerate gypsy-like LTR retrotransposon in the filamentous ascomycete *Podospora anserina*." *Curr Genet* **38**(3): 132-140.

- Lalucque, H. and P. Silar (2000). "In vivo labelling of functional ribosomes reveals spatial regulation during starvation in *Podospora anserina*." *BMC Genet* **1**(1): 3.

- Loubradou, G. and B. Turcq (2000). "Vegetative incompatibility in filamentous fungi: a roundabout way of understanding the phenomenon." *Res Microbiol* **151**(4): 239-245.

- Osiewacz, H. D. (2000). "The genetic basis of aging in the fungal aging model *Podospora anserina*." *FUTURA* **15**: 237-241.

- Osiewacz, H. D. and C. Borghouts (2000). "Mitochondrial oxidative stress and aging in the filamentous fungus *Podospora anserina*." *Ann N Y Acad Sci* **908**: 31-39.

- Osiewacz, H. D. and C. Borghouts (2000). "Cellular copper homeostasis, mitochondrial DNA instabilities, and lifespan control in the filamentous fungus *Podospora anserina*." *Exp Gerontol* **35**(6-7): 677-686.

- Raju, N. B. and D. D. Perkins (2000). "Programmed ascospore death in the homothallic ascomycete Coniochaeta tetrasporas." *Fungal Genet Biol* **30**(3): 213-221.

- Saguez, C., G. Lecellier, et al. (2000). "Intronic GIY-YIG endonuclease gene in the mitochondrial genome of *Podospora curvicolla* : evidence for mobility." *Nucleic Acids Res* **28**: 1299-1306.

- Saupe, S. J. (2000). "Molecular genetics of heterokaryon incompatibility in filamentous ascomycetes." *Microbiol Mol Biol Rev* **64**(3): 489-502.

- Saupe, S. J., C. Clave, et al. (2000). "Vegetative incompatibility in filamentous fungi: *Podospora* and *Neurospora* provide some clues." *Curr Opin Microbiol* **3**(6): 608-612.

- Saupe, S. J., C. Clavé, et al. (2000). "Characterization of *hch*, the *Podospora anserina* homolog of the *het-c* heterokaryon incompatibility gene of *Neurospora crassa*." *Curr Genet* **38**(1): 39-47.

- Sellem, C. H., O. Begel, et al. (2000). "Recombinant mitochondrial DNA molecules suggest a template switching ability for group-II-intron reverse transcriptase." *Curr Genet* **37**(1): 24-28.

- Silar, P., M. Rossignol, et al. (2000). "Deletion and dosage modulation of the *eEF1A* gene in *Podospora anserina*: effect on the life cycle." *Biogerontology* **1**(1): 47-54.

- Silar, P., M. Rossignol, et al. (2000). "Informational suppressor alleles of the *eEF1A* gene, fertility and cell degeneration in *Podospora anserina*." *Mol Gen Genet* **264**(3): 354-362.
- van der Gaag, M., A. J. M. Debets, et al. (2000). "Spore-killing meiotic drive factors in a natural population of the fungus *Podospora anserina*." *Genetics* **156**(2): 593-605.

- Wang, Y. Z. (2000). "The genus Podospora in Taiwan." *Mycotaxon* **76**: 373-391.

- Arnaise, S., D. Zickler, et al. (2001). "Mutations in mating-type genes of the heterothallic fungus *Podospora anserina* lead to self-fertility." *Genetics* **159**(2): 545-556.

- Arnaise, S., D. Zickler, et al. (2001). "*pah1*: a homeobox gene involved in hypha morphology and microconidiogenesis in the filamentous ascomycete *Podospora anserina*." *Mol Microbiol* **39**(1): 54-64.

- Averbeck, N. B., C. Borghouts, et al. (2001). "Molecular control of copper homeostasis in filamentous fungi: increased expression of a metallothionein gene during aging of *Podospora anserina*." *Mol Gen Genet* **264**(5): 604-612.

- Borghouts, C., A. Werner, et al. (2001). "Copper-modulated gene expression and senescence in the filamentous fungus *Podospora anserina*." *Mol Cell Biol* **21**(2): 390-399.

- Coustou-Linares, V., M. L. Maddelein, et al. (2001). "In vivo aggregation of the HET-s prion protein of the fungus *Podospora anserina*." *Mol Microbiol* **42**(5): 1325-1335.

- Dettman, J. R., F. M. Harbinski, et al. (2001). "Ascospore morphology is a poor predictor of the phylogenetic relationships of neurospora and gelasinospora." *Fungal Genetics and Biology* **34**: 49-61.

- Graia, F., O. Lespinet, et al. (2001). "Genome quality control: RIP (repeat-induced point mutation) comes to Podospora." *Mol Microbiol* **40**(3): 586-595.

- Koll, F., C. Sidoti, et al. (2001). "Mitochondrial membrane potential and ageing in *Podospora anserina*." *Mech Ageing Dev* **122**(2): 205-217.

- Lorenzo, L. E., M. Havrylenko, et al. (2001). "The Genera Arnium and Podospora from Argentina." *Mycologia* **93**(6): 1221-1230.

- Lorin, S., E. Dufour, et al. (2001). "Overexpression of the alternative oxidase restores senescence and fertility in a long-lived respiration-deficient mutant of *Podospora anserina*." *Mol Microbiol* **42**(5): 1259-1267.

- Osiewacz, H. D. and S. W. Stumpferl (2001). "Metabolism and aging in the filamentous fungus *Podospora anserina*." *Arch Gerontol Geriatr* **32**(3): 185-197.

- Paoletti, M., M. Castroviejo, et al. (2001). "Identification and characterization of a gene encoding a subtilisin- like serine protease induced during the vegetative incompatibility reaction in *Podospora anserina*." *Curr Genet* **39**(4): 244-252.

- Richardson, M. J. (2001). "Coprophilous Fungi from Brazil." *Brazilian Archives of Biology and Technology* **44**(3): 283-289.

- Silar, P., H. Lalucque, et al. (2001). "*eEF1A* Controls ascospore differentiation through elevated accuracy, but controls longevity and fruiting body formation through another mechanism in *Podospora anserina*." *Genetics* **158**(4): 1477-1489.

- Silar, P., H. Lalucque, et al. (2001). "Cell degeneration in the model system *Podospora anserina*." *Biogerontology* **2**(1): 1-17.

- Albert, B. and C. H. Sellem (2002). "Dynamics of the mitochondrial genome during *Podospora anserina* aging." *Curr Genet* **40**(6): 365-373.

- Barreau, C., C. Sellem, et al. (2002). "A rapid and efficient method using chromoslots to assign any newly cloned DNA sequence to its cognate chromosome in the filamentous fungus *Podospora anserina*." *FEMS Microbiol Lett* **216**(1): 55-60.

- Borghouts, C., C. Q. Scheckhuber, et al. (2002). "Copper homeostasis and aging in the fungal model system *Podospora anserina*: differential expression of *PaCtr3* encoding a copper transporter." *Int J Biochem Cell Biol* **34**(11): 1355-1371.

- Borghouts, C., C. Q. Scheckhuber, et al. (2002). "Respiration, copper availability and SOD activity in *P. anserina* strains with different lifespan." *Biogerontology* **3**(3): 143-153.

- Bouex, P., M. Sabourin, et al. (2002). "Purification and characterization of an endo-exonuclease from *Podospora anserina* mitochondria." *Biochim Biophys Acta* **1574**(1): 72-84.

- Coppin, E. (2002). "The *fle1* gene encoding a C2H2 zinc finger protein co-ordinates male and female sexual differentiation in *Podospora anserina*." *Mol Microbiol* **43**(5): 1255-1268.

- Dequard-Chablat, M. and C. Alland (2002). "Two copies of *mthmg1*, encoding a novel mitochondrial HMG-like protein, delay accumulation of mitochondrial DNA deletions in *Podospora anserina*." *Eukaryot Cell* **1**(4): 503-513.

- Dos Reis, S., B. Coulary-Salin, et al. (2002). "The HET-s prion protein of the filamentous fungus *Podospora anserina* aggregates in *vitro* into amyloid-like fibrils." *J Biol Chem* **277**(8): 5703-5706.

- Espagne, E., P. Balhadere, et al. (2002). "HET-E and HET-D belong to a new subfamily of WD40 proteins involved in vegetative incompatibility specificity in the fungus *Podospora anserina*." *Genetics* **161**(1): 71-81.

- Liebman, S. W. (2002). "Progress toward an ultimate proof of the prion hypothesis." *Proc Natl Acad Sci U S A* **99**(14): 9098-9100.

- Maddelein, M. L., S. Dos Reis, et al. (2002). "Amyloid aggregates of the HET-s prion protein are infectious." *Proc Natl Acad Sci U S A* **99**(11): 7402-7407.

- Osiewacz, H. D. (2002). "Aging in fungi: role of mitochondria in *Podospora anserina*." *Mech Ageing Dev* **123**(7): 755-764.

- Osiewacz, H. D. (2002). "Mitochondrial functions and aging." *Gene* **286**(1): 65-71.

- Osiewacz, H. D. (2002). "Genes, mitochondria and aging in filamentous fungi." *Ageing Res Rev* **1**(3): 425-442.

- Ruprich-Robert, G., V. Berteaux-Lecellier, et al. (2002). "Identification of six loci in which mutations partially restore peroxisome biogenesis and/or alleviate the metabolic defect of pex2 mutants in Podospora." *Genetics* **161**(3): 1089-1099.
- Ruprich-Robert, G., D. Zickler, et al. (2002). "Lack of mitochondrial citrate synthase discloses a new meiotic checkpoint in a strict aerobe." *EMBO J* **21**(23): 6440-6451.

- Uptain, S. M. and S. Lindquist (2002). "Prions as protein-based genetic elements." *Annu. Rev. Microbiol.* **56**: 703-741.

- Wickner, R. B., H. K. Edskes, et al. (2002). "Prions of yeast as epigenetic phenomena: high protein "copy number" inducing protein "silencing"." *Adv Genet* **46**: 485-525.

- Balguerie, A., S. Dos Reis, et al. (2003). "Domain organization and structure-function relationship of the HET-s prion protein of *Podospora anserina*." *EMBO J* **22**(9): 2071-2081.

- Boisnard, S., D. Zickler, et al. (2003). "Overexpression of a human and a fungal ABC transporter similarly suppresses the differentiation defects of a fungal peroxisomal mutant but introduces pleiotropic cellular effects." *Mol. Microbiol.* **49**(5): 1287-1296.

- Dalstra, H. J. P., K. Swart, et al. (2003). "Sexual transmission of the [Het-s] prion leads to meiotic drive in *Podospora anserina*." *Proc Natl Acad Sci U S A* **100**(11): 6616-6621.

- Dementhon, K., M. Paoletti, et al. (2003). "Rapamycin Mimics the Incompatibility Reaction in the Fungus *Podospora anserina*." *Eukaryot Cell* **2**(2): 238-246.

- Lalucque, H. and P. Silar (2003). "NADPH oxidase: an enzyme for multicellularity?" *Trends Microbiol* **11**(1): 9-12.

- Laquel-Robert, P. and M. Castroviejo (2003). "Stimulation of a mitochondrial endo-exonuclease from *Podospora anserina* by PCNA." *Biochem Biophys Res Commun* **303**(2): 713-720.

- Malagnac, F. and P. Silar (2003). "Non-mendelian determinants of morphology in fungi." *Cur. Opinion in Microbiol.* **6**: 641-645.

- Mattjus, P., B. Turcq, et al. (2003). "Glycolipid intermembrane transfer is accelerated by HET-C2, a filamentous fungus gene product involved in the cell-cell incompatibility response." *Biochemistry* **42**(2): 535-542.

- Nazabal, A., S. Dos Reis, et al. (2003). "Conformational transition occurring upon amyloid aggregation of the HET-s prion protein of *Podospora anserina* analyzed by hydrogen/deuterium exchange and mass spectrometry." *Biochemistry* **42**(29): 8852-8861.

- Perkins, D. D. (2003). "A fratricidal fungal prion." *Proc Natl Acad Sci U S A* **100**(11): 6292-6294.

- Pinan-Lucarre, B., M. Paoletti, et al. (2003). "Autophagy is induced during cell death by incompatibility and is essential for differentiation in the filamentous fungus *Podospora anserina*." *Mol Microbiol* **47**(2): 321-333.

- Prokhorov, V. P. and N. L. Armenskaya (2003). "The genus *Podospora* Ces. (Sordariales, Pyrenomycetes) in the European Russia." *Bull. Moscow Soc. Natur. Biol. Ser.* **108** (3): 51-58.

- Silar, P., C. Barreau, et al. (2003). "Characterization of the genomic organization of the region bordering the centromere of chromosome V of *Podospora anserina* by direct sequencing." *Fungal Genet Biol* **39**(3): 250-263.

- van der Gaag, M., A. J. M. Debets, et al. (2003). "Spore killing in the fungus *Podospora anserina*: a connection between meiotic drive and vegetative incompatibility?" *Genetica* **117**(1): 59-65.

- Balguerie, A., S. Dos Reis, et al. (2004). "The sequences appended to the amyloid core region of the HET-s prion protein determine higher-order aggregate organization in vivo." *J Cell Sci* **117**(Pt 12): 2599-2610.

- Baxa, U., K. L. Taylor, et al. (2004). "Prions of Saccharomyces and *Podospora*." *Contrib Microbiol* **11**: 50-71.

- Bouhouche, K., D. Zickler, et al. (2004). "Altering a Gene Involved in Nuclear Distribution Increases the Repeat-Induced Point Mutation Process in the Fungus *Podospora anserina*." *Genetics* **167**(1): 151-159.

- Contamine, V., D. Zickler, et al. (2004). "The *Podospora rmp1* gene implicated in nucleus-mitochondria cross-talk encodes an essential protein whose subcellular location is developmentally regulated." *Genetics* **166**(1): 135-150.

- Dementhon, K., S. J. Saupe, et al. (2004). "Characterization of IDI-4, a bZIP transcription factor inducing autophagy and cell death in the fungus *Podospora anserina*." *Mol Microbiol* **53**(6): 1625-1640.

- Dufour, E. and N. G. Larsson (2004). "Understanding aging: revealing order out of chaos." *Biochim Biophys Acta* **1658**(1-2): 122-132.

- Hamann, A. and H. D. Osiewacz (2004). "Genetic analysis of spore killing in the filamentous ascomycete *Podospora anserina*." *Fungal Genetics and Biology* **41**(12): 1088-1098.

- Huhndorf, S. M., A. N. Miller, et al. (2004). "Molecular systematics of the Sordariales: the order and the family Lasiosphaeriaceae redefined." *Mycologia* **96**(2): 368-387.

- Kicka, S. and P. Silar (2004). "PaASK1, a Mitogen-Activated Protein Kinase Kinase That Controls Cell Degeneration and Cell Differentiation in *Podospora anserina*." *Genetics* **166**(3): 1241-1252.

- Krause, F., C. Q. Scheckhuber, et al. (2004). "Supramolecular Organization of Cytochrome c Oxidase- and Alternative Oxidase- dependent Respiratory Chains in the Filamentous Fungus *Podospora anserina*." *J. Biol. Chem.* **279**(25): 26453-26461.

- Lalucque, H. and P. Silar (2004). "Incomplete penetrance and variable expressivity of a growth defect as a consequence of knocking out two K(+) transporters in the euascomycete fungus *Podospora anserina*." *Genetics* **166**(1): 125-133.

- Maas, M. F., H. J. Boer, et al. (2004). "The mitochondrial plasmid pAL2-1 reduces calorie restriction mediated life span extension in the filamentous fungus *Podospora anserina*." *Fungal Genet Biol* **41**(9): 865-871.

- Malagnac, F., H. Lalucque, et al. (2004). "Two NADPH oxidase isoforms are required for sexual reproduction and ascospore germination in the filamentous fungus *Podospora anserina*." *Fungal Genetics & Biology* **41**(11): 982-997.

- Richardson, M. J. (2004). "Coprophilous fungi from Morocco." *Botanical Journal of Scotland* **56**(2): 147-162.
- Stumpferl, S. W., O. Stephan, et al. (2004). "Impact of a disruption of a pathway delivering copper to mitochondria on *Podospora anserina* metabolism and life span." *Eukaryot Cell* **3**(1): 200-211.

- Butler, M. I., T. J. Goodwin, et al. (2005). "Two new fungal inteins." *Yeast* **22**(6): 493-501.

- cai, L., R. Jeewon, et al. (2005). "Phylogenetic evaluation and taxonomic revision of Schizothecium based on ribosomal DNA and protein coding genes." *Fung. Div.* **19**: 1-21.

- Coppin, E., C. de Renty, et al. (2005). "The Function of the Coding Sequences for the Putative Pheromone Precursors in *Podospora anserina* Is Restricted to Fertilization." *Eukaryot Cell* **4**(2): 407-420.

- Dalstra, H. J., R. van der Zee, et al. (2005). "Non-mendelian inheritance of the HET-s prion or HET-s prion domains determines the het-S spore killing system in *Podospora anserina*." *Fungal Genet Biol* **42**(10): 836-847.

- Dementhon, K. and S. J. Saupe (2005). "DNA-Binding Specificity of the IDI-4 Basic Leucine Zipper Factor of *Podospora anserina* Defined by Systematic Evolution of Ligands by Exponential Enrichment (SELEX)." *Eukaryot Cell* **4**(2): 476-483.

- Dobson, C. M. (2005). "Structural biology: prying into prions." *Nature* **435**(7043): 747-749.

- Fedorova, N. D., J. H. Badger, et al. (2005). "Comparative analysis of programmed cell death pathways in filamentous fungi." *BMC Genomics* **6**(1): 177.

- Haedens, V., F. Malagnac, et al. (2005). "Genetic control of an epigenetic cell degeneration syndrome in *Podospora anserina*." *Fungal Genetics & Biology* **42**(6): 564-577.

- Hamann, A., K. Krause, et al. (2005). "A two-step protocol for efficient deletion of genes in the filamentous ascomycete *Podospora anserina*." *Curr Genet* **48**(4): 270-275.

- Juvvadi, P. R., Y. Seshime, et al. (2005). "Genomics reveals traces of fungal phenylpropanoid-flavonoid metabolic pathway in the filamentous fungus Aspergillus oryzae." *J Microbiol* **43**(6): 475-486.

- Liebman, S. W. (2005). "Structural clues to prion mysteries." *Nat Struct Mol Biol* **12**(7): 567-568.

- Lombardi, L. M. and S. Brody (2005). "Circadian rhythms in Neurospora crassa: Clock gene homologues in fungi." *Fungal Genet Biol* **42**(11): 887-892.

- Miller, A. N. and S. M. Huhndorf (2005). "Multi-gene phylogenies indicate ascomal wall morphology is a better predictor of phylogenetic relationships than ascospore morphology in the *Sordariales* (*Ascomycota*, *Fungi*)." *Molecular Phylogenetics and Evolution* **35**(1): 60-75.

- Money, N. P. (2005). "Fungal irritability and survival mechanisms." *Mycol. Res.* **109**: 129.

- Nazabal, A., M. Bonneu, et al. (2005). "High-resolution H/D exchange studies on the HET-s218-295 prion protein." *J Mass Spectrom* **40**(5): 580-590.

- Nazabal, A., M. L. Maddelein, et al. (2005). "Probing the structure of the infectious amyloid form of the prion-forming domain of HET-s using high resolution hydrogen/deuterium exchange monitored by mass spectrometry." *J Biol Chem* **280**(14): 13220-13228.

- Pinan-Lucarre, B., A. Balguerie, et al. (2005). "Accelerated Cell Death in Podospora Autophagy Mutants." *Eukaryot Cell* **4**(11): 1765-1774.

- Ritter, C., M. L. Maddelein, et al. (2005). "Correlation of structural elements and infectivity of the HET-s prion." *Nature* **435**(7043): 844-848.

- Sellem, C. H., C. Lemaire, et al. (2005). "Interaction Between the oxa1 and rmp1 Genes Modulates Respiratory Complex Assembly and Life Span in *Podospora anserina*." *Genetics* **169**(3): 1379-1389.

- Seshime, Y., P. R. Juvvadi, et al. (2005). "Discovery of a novel superfamily of type III polyketide synthases in Aspergillus oryzae." *Biochem Biophys Res Commun* **331**(1): 253-260.

- Silar, P. (2005). "Peroxide accumulation and cell death in filamentous fungi induced by contact with a contestant." *Mycolological Research* **109**: 137-149.

- Airenne, T. T., H. Kidron, et al. (2006). "Structural evidence for adaptive ligand binding of glycolipid transfer protein." *J Mol Biol* **355**(2): 224-236.

- Benkemoun, L., R. Sabate, et al. (2006). "Methods for the in vivo and in vitro analysis of [Het-s] prion infectivity." *Methods* **39**(1): 61-67.

- Benkemoun, L. and S. J. Saupe (2006). "Prion proteins as genetic material in fungi." *Fungal Genetics and Biology* **43**(12): 789-803.

- Bonnet, C., E. Espagne, et al. (2006). "The peroxisomal import proteins PEX2, PEX5 and PEX7 are differently involved in *Podospora anserina* sexual cycle." *Mol Microbiol* **62**(1): 157-169.

- Boye-Harnasch, M. and C. Cullin (2006). "A novel in vitro filter trap assay identifies tannic acid as an amyloid aggregation inducer for HET-s." *J Biotechnol* **125**: 222-230.

- Cai, L., R. Jeewon, et al. (2006). "Molecular systematics of Zopfiella and allied genera: evidence from multi-gene sequence analyses." *Mycological Research* **110**(Pt 4): 359-368.

- Dequard-Chablat, M. and P. Silar (2006). "*Podospora anserina* AS6 gene encodes the cytosolic ribosomal protein of the E. coli S12 family." *Fung. Genet. Newslet.* **53**: 26-29.

- Glass, N. L. and K. Dementhon (2006). "Non-self recognition and programmed cell death in filamentous fungi." *Current Opinion in Microbiology* **9**(6): 553-558.
- Gredilla, R., J. Grief, et al. (2006). "Mitochondrial free radical generation and lifespan control in the fungal aging model *Podospora anserina*." *Exp Gerontol* **41**(4): 439-447.

- Hu, D., L. Cai, et al. (2006). "The genera *Podospora* and *Schizothecium* from Mainland China." *Cryptogamie, Mycologie* **27**(2): 1-22.

- Kicka, S., C. Bonnet, et al. (2006). "A mitotically inheritable unit containing a MAP kinase module." *Proceeding of the National Academy of Science, U. S. A.* **103**(36): 13445-13450.

- Krause, F., C. Q. Scheckhuber, et al. (2006). "OXPHOS Supercomplexes: respiration and life-span control in the aging model *Podospora anserina*." *Ann N Y Acad Sci* **1067**: 106-115.

- Liu, Y., C. Ritter, et al. (2006). "The formation of bioactive amyloid species by prion proteins in vitro and in cells." *Neurosci Lett* **406**(3): 200-204.

- Lorin, S., E. Dufour, et al. (2006). "Mitochondrial metabolism and aging in the filamentous fungus *Podospora anserina*." *Biochim Biophys Acta* **1757**: 604-610.

- Malagnac, F. and P. Silar (2006). "Regulation, cell differentiation and protein-based inheritance." *Cell Cycle* **5**(22): 2584-2587.

- Masunga, G. S., Ø. Andresen, et al. (2006). "Elephant dung decomposition and coprophilous fungi in two habitats of semi-arid Botswana." *Mycol Res* **110**(10): 1214-1226.

- Nazabal, A. and J. M. Schmitter (2006). "Hydrogen-deuterium exchange analyzed by matrix-assisted laser desorption-ionization mass spectrometry and the HET-s prion model." *Methods Enzymol* **413**: 167-181.

- Osiewacz, H. D. and C. Q. Scheckhuber (2006). "Impact of ROS on ageing of two fungal model systems: Saccharomyces cerevisiae and *Podospora anserina*." *Free Radic Res* **40**(12): 1350-1358.

- Pinan-Lucarre, B., I. Iraqui, et al. (2006). "*Podospora anserina* target of rapamycin." *Curr Genet* **50**(1): 23-31.

- Scheckhuber, C. and H. D. Osiewacz (2006). "The role of mitochondria in conserved mechanisms of aging." *Sci Aging Knowledge Environ* **2006**(10): pe15.

- Siemer, A. B., A. A. Arnold, et al. (2006). "Observation of highly flexible residues in amyloid fibrils of the HET-s prion." *J Am Chem Soc* **128**(40): 13224-13228.

- Siemer, A. B., C. Ritter, et al. (2006). "13C, 15N resonance assignment of parts of the HET-s prion protein in its amyloid form." *J Biomol NMR* **34**(2): 75-87.

- Baxa, U., R. B. Wickner, et al. (2007). "Characterization of beta-sheet structure in Ure2p1-89 yeast prion fibrils by solid-state nuclear magnetic resonance." *Biochemistry* **46**(45): 13149-13162.

- Coppin, E. and P. Silar (2007). "Identification of PaPKS1, a polyketide synthase involved in melanin formation and its use as a genetic tool in *Podospora anserina*." *Mycological Research* **111**(Pt 8): 901-908.

- Groebe, K., F. Krause, et al. (2007). "Differential proteomic profiling of mitochondria from *Podospora anserina*, rat and human reveals distinct patterns of age-related oxidative changes." *Exp Gerontol* **42**(9): 887-898.

- Hamann, A., D. Brust, et al. (2007). "Deletion of putative apoptosis factors leads to lifespan extension in the fungal ageing model *Podospora anserina*." *Mol Microbiol* **65**(4): 948-958.

- Jamet-Vierny, C., R. Debuchy, et al. (2007). "IDC1, a Pezizomycotina-specific gene that belongs to the PaMpk1 MAP kinase transduction cascade of the filamentous fungus *Podospora anserina*." *Fungal Genetics & Biology* **44**(12): 1219-1230.

- Laquel-Robert, P., C. H. Sellem, et al. (2007). "Identification and biochemical analysis of a mitochondrial endonuclease of *Podospora anserina* related to curved-DNA binding proteins." *Biochim Biophys Acta* **1770**(4): 527-542.

- Maas, M. F., R. F. Hoekstra, et al. (2007). "A mitochondrial mutator plasmid that causes senescence under dietary restricted conditions." *BMC Genet* **8**: 9.

- Maas, M. F., C. H. Sellem, et al. (2007). "Integration of a pAL2-1 homologous mitochondrial plasmid associated with life span extension in *Podospora anserina*." *Fungal Genet Biol* **44**(7): 659-671.

- Malagnac, F., B. Klapholz, et al. (2007). "PaTrx1 and PaTrx3, two cytosolic thioredoxins of the filamentous ascomycete *Podospora anserina* involved in sexual development and cell degeneration." *Eukaryot Cell* **6**: 2323-2331.

- Malato, L., S. Dos Reis, et al. (2007). "Role of Hsp104 in the propagation and inheritance of the [Het-s] prion." *Mol Biol Cell* **18**(12): 4803-4812.

- Martins, M., P. Silar, et al. (2007). "Cloning, and functional characterization of two NAT enzymes in the soil fungus *Podospora anserina*." *FEBS J.* **274**: 226.

- Paoletti, M. and C. Clave (2007). "The fungus-specific HET domain mediates programmed cell death in *Podospora anserina*." *Eukaryot Cell* **6**(11): 2001-2008.

- Paoletti, M., S. J. Saupe, et al. (2007). "Genesis of a fungal non-self recognition repertoire." *PLoS ONE* **2**(3): e283.

- Pinan-Lucarre, B., M. Paoletti, et al. (2007). "Cell death by incompatibility in the fungus *Podospora*." *Semin Cancer Biol* **17**(2): 101-111.

- Sabate, R., U. Baxa, et al. (2007). "Prion and non-prion amyloids of the HET-s prion forming domain." *J Mol Biol* **370**(4): 768-783.

- Sabate, R. and S. J. Saupe (2007). "Thioflavin T fluorescence anisotropy: an alternative technique for the study of amyloid aggregation." *Biochem Biophys Res Commun* **360**(1): 135-138.

- Saupe, S. J. (2007). "A Short History of Small s." *Prion* **1**(2): 110-115.
- Scheckhuber, C. Q., N. Erjavec, et al. (2007). "Reducing mitochondrial fission results in increased life span and fitness of two fungal ageing models." *Nat Cell Biol* 9(1): 99-105.

- Sellem, C. H., S. Marsy, et al. (2007). "A mutation in the gene encoding cytochrome c1 leads to a decreased ROS content and to a long-lived phenotype in the filamentous fungus *Podospora anserina*." *Fungal Genetics & Biology* 44(7): 648-658.

- Sen, A., U. Baxa, et al. (2007). "Mass analysis by scanning transmission electron microscopy and electron diffraction validate predictions of stacked beta-solenoid model of HET-s prion fibrils." *J Biol Chem* 282(8): 5545-5550.

- Shkundina, I. S. and M. D. Ter-Avanesyan (2007). "Prions." *Biochemistry (Mosc)* 72(13): 1519-1536.

- Taneja, V., M. L. Maddelein, et al. (2007). "A non-Q/N-rich prion domain of a foreign prion, [Het-s], can propagate as a prion in yeast." *Mol Cell* 27(1): 67-77.

- Wickner, R. B., H. K. Edskes, et al. (2007). "Prions of fungi: inherited structures and biological roles." *Nat Rev Microbiol* 5(8): 611-618.

- Wickner, R. B., H. K. Edskes, et al. (2007). "Prions of fungi: inherited structures and biological roles." *Nature Reviews Microbiology* 5: 611.

- Anisimov, V. N., L. E. Bakeeva, et al. (2008). "Mitochondria-targeted plastoquinone derivatives as tools to interrupt execution of the aging program. 5. SkQ1 prolongs lifespan and prevents development of traits of senescence." *Biochemistry (Mosc)* 73(12): 1329-1342.

- Arnaise, S., D. Zickler, et al. (2008). "Mutations in mating-type genes greatly decrease repeat-induced point mutation process in the fungus *Podospora anserina*." *Fungal Genet Biol* 45(3): 207-220.

- Boivin, A., S. Gaumer, et al. (2008). "Life span extension by dietary restriction is reduced but not abolished by loss of both SIR2 and HST2 in *Podospora anserina*." *Mech Ageing Dev* 129: 714-721.

- Doveri, F. (2008). "A bibliography of *Podospora* and *Schizothecium*, a key to the species, and a description of *Podospora dasypogon* newly recorded from Italy." *PAGINE DI MICROLOGIA* 29: 61-159.

- El-Khoury, R., C. H. Sellem, et al. (2008). "Gene deletion and allelic replacement in the filamentous fungus *Podospora anserina*." *Curr Genet* 53: 249-258.

- Espagne, E., O. Lespinet, et al. (2008). "The genome sequence of the model ascomycete fungus *Podospora anserina*." *Genome Biology* 9(5): R77.

- Hamann, A., D. Brust, et al. (2008). "Apoptosis pathways in fungal growth, development and ageing." *Trends in Microbiology* 16(6): 276-283.

- Kunstmann, B. and H. D. Osiewacz (2008). "Over-expression of an S-adenosylmethionine-dependent methyltransferase leads to an extended lifespan of *Podospora anserina* without impairments in vital functions." *Aging Cell* 7(5): 651-662.

- Lambou, K., F. Malagnac, et al. (2008). "The crucial role during ascospore germination of the Pls1 tetraspanin in *Podospora anserina* provides an example of the convergent evolution of morphogenetic processes in fungal plant pathogens and saprobes." *Eukaryotic Cell* 7: 1809-1818.

- Malagnac, F., F. Bidard, et al. (2008). "Convergent evolution of morphogenetic processes in fungi: Role of tetraspanins and NADPH oxidases 2 in plant pathogens and saprobes." *Comm. int. Biol.* 1(2): 181-182.

- Pain, A. and C. Hertz-Fowler (2008). "Genomic adaptation: a fungal perspective." *Nat Rev Microbiol* 6(8): 572-573.

- Paoletti, M. and S. J. Saupe (2008). "The genome sequence of *Podospora anserina*, a classic model fungus." *Genome Biol* 9(5): 223.

- Park, J., S. Lee, et al. (2008). "Fungal cytochrome P450 database." *BMC Genomics* 9: 402.

- Peraza-Reyes, L., D. Zickler, et al. (2008). "The Peroxisome RING-Finger Complex is Required for Meiocyte Formation in the Fungus *Podospora anserina*." *Traffic* 9: 1998-2009.

- Pinan-Lucarre, B. and C. Clave (2008). "Monitoring autophagy in the filamentous fungus *Podospora anserina*." *Methods Enzymol* 451: 251-270.

- Poggeler, S., B. Hoff, et al. (2008). "Asexual cephalosporin C producer Acremonium chrysogenum carries a functional mating type locus." *Appl Environ Microbiol* 74(19): 6006-6016.

- Reblova, M. (2008). "Bellojisia, a New Sordariaceous Genus for Jobellisia rhynchostoma and a Description of Jobellisiaceae Fam. Nov." *Mycologia* 100(6): 893-901.

- Richardson, M. J. (2008). "Records of Coprophilous Fungi from the Lesser Antilles and Puerto Rico." *Caribbean Journal of Science* 44(2): 206-214.

- Sabate, R., I. Lascu, et al. (2008). "On the binding of Thioflavin-T to HET-s amyloid fibrils assembled at pH 2." *J Struct Biol* 162(3): 387-396.

- Scheckhuber, C. Q. and H. D. Osiewacz (2008). "*Podospora anserina*: a model organism to study mechanisms of healthy ageing." *Mol Genet Genomics* 280: 365-374.

- Scheckhuber, C. Q., E. Rodel, et al. (2008). "Regulation of mitochondrial dynamics--characterization of fusion and fission genes in the ascomycete *Podospora anserina*." *Biotechnol J* 3(6): 781-790.

- van Diepeningen, A. D., A. J. Debets, et al. (2008). "Mitochondrial pAL2-1 plasmid homologs are senescence factors in *Podospora anserina* independent of intrinsic senescence." *Biotechnol J* 3(6): 791-802.