bluuebunny/crossref_metadata_2025_split huggingface dataset:
Testing Natural Selection vs. Genetic Drift in Phenotypic Evolution Using Quantitative Trait Locus Data
Authors: Orr H Allen 
Published: April 2021

Abstract
Evolutionary biologists have long sought a way to determine whether a phenotypic difference between two taxa was caused by natural selection or random genetic drift. Here I argue that data from quantitative trait locus (QTL) analyses can be used to test the null hypothesis of neutral phenotypic evolution. I propose a sign test that compares the observed number of plus and minus alleles in the “high line” with that expected under neutrality, conditioning on the known phenotypic difference between the taxa. Rejection of the null hypothesis implies a role for directional natural selection. This test is applicable to any character in any organism in which QTL analysis can be performed.
The [KIL-d] Cytoplasmic Genetic Element of Yeast Results in Epigenetic Regulation of Viral M Double-Stranded RNA Gene Expression
Authors: Tallóczy Zsolt , Menon Sujoy , Neigeborn Lenore , Leibowitz Michael J 
Published: April 2021

Abstract
[KIL-d] is a cytoplasmically inherited genetic trait that causes killer virus-infected cells of Saccharomyces cerevisiae to express the normal killer phenotypes in a/α cells, but to show variegated defective killer phenotypes in a or α type cells. Mating of [KIL-d] haploids results in “healing” of their phenotypic defects, while meiosis of the resulting diploids results in “resetting” of the variegated, but mitotically stable, defects. We show that [KIL-d] does not reside on the double-stranded RNA genome of killer virus. Thus, the [KIL-d] effect on viral gene expression is epigenetic in nature. Resetting requires nuclear events of meiosis, since [KIL-d] can be cytoplasmically transmitted during cytoduction without causing defects in killer virus expression. Subsequently, mating of these cytoductants followed by meiosis generates spore clones expressing variegated defective phenotypes. Cytoduction of wild-type cytoplasm into a phenotypically defective [KIL-d] haploid fails to heal, nor does simultaneous or sequential expression of both MAT alleles cause healing. Thus, healing is not triggered by the appearance of heterozygosity at the MAT locus, but rather requires the nuclear fusion events which occur during mating. Therefore, [KIL-d] appears to interact with the nucleus in order to exert its effects on gene expression by the killer virus RNA genome.
The Female-Determining Gene F of the Housefly, Musca domestica, Acts Maternally to Regulate Its Own Zygotic Activity
Authors: Dübendorfer Andreas , Hediger Monika 
Published: April 2021

Abstract
In Musca domestica, the common housefly, female development requires the continuous activity of the sex-determining gene F from early embryogenesis until metamorphosis. To activate F in embryogenesis, two conditions must be met: There must be no male-determining M factor in the zygotic genome, and the egg must be preconditioned by F activity in the maternal germ line. This maternal activity can be suppressed by introducing an M factor into the maternal germ line, which causes all offspring, including those that do not carry M, to develop as males. By transplantation of pole cells (germline progenitor cells) we have constructed such females with a genetically male germ line and, simultaneously, males with a genetically female germ line carrying a constitutive allele of F [FDominant (FD)]. Crosses between these animals yielded offspring that, despite the presence of M in the maternal germ line, were of female sex, solely due to zygotic FD brought in via the sperm. This shows that zygotic F function alone is sufficient to promote female development and that in the wild-type situation, maternal F product serves no other function but to activate the zygotic F gene.
Interactions Among Dosage-Dependent Trans-Acting Modifiers of Gene Expression and Position-Effect Variegation in Drosophila
Authors: Bhadra Utpal , Bhadra Manika Pal , Birchler James A 
Published: April 2021

Abstract
We have investigated the effect of dosage-dependent trans-acting regulators of the white eye color gene in combinations to understand their interaction properties. The consequences of the interactions will aid in an understanding of aneuploid syndromes, position-effect variegation (PEV), quantitative traits, and dosage compensation, all of which are affected by dosage-dependent modifiers. Various combinations modulate two functionally related transcripts, white and scarlet, differently. The overall trend is that multiple modifiers are noncumulative or epistatic to each other. In some combinations, developmental transitions from larvae to pupae to adults act as a switch for whether the effect is positive or negative. With position-effect variegation, similar responses were found as with gene expression. The highly multigenic nature of dosage-sensitive modulation of both gene expression and PEV suggests that dosage effects can be progressively transduced through a series of steps in a hierarchical manner.
Molecular Evolution of Two Lineages of L1 (LINE-1) Retrotransposons in the California Mouse, Peromyscus californicus
Authors: Casavant N Carol , Lee Rhonda N , Sherman Amy N , Wichman Holly A 
Published: April 2021

Abstract
The large number of L1 [long interspersed elements (LINE)-1] sequences found in the genome is due to the insertion of copies of the retrotransposon over evolutionary time. The majority of copies appear to be replicates of a few active, or “master” templates. A continual replacement of master templates over time gives rise to lineages distinguishable by their own unique set of shared-sequence variants. A previous analysis of L1 sequences in deer mice, Peromyscus maniculatus and P. leucopus, revealed two active L1 lineages, marked by different rates of evolution, whose most recent common ancestor predates the expansion of the Peromyscus species. Here we exploit lineage-specific, shared-sequence variants to reveal a paucity of Lineage 2 sequences in at least one species, P. californicus. The dearth of Lineage 2 copies in P. californicus suggests that Lineage 2 may have been unproductive until after the most recent common ancestor of P. californicus and P. maniculatus. We also show that Lineage 1 appears to have a higher rate of evolution in P. maniculatus relative to either P. californicus or P. leucopus. As a phylogenetic tool, L1 lineage-specific variants support a close affinity between P. californicus and P. eremicus relative to the other species examined.
The Association of Flowering Time Quantitative Trait Loci with Duplicated Regions and Candidate Loci in Brassica oleracea
Authors: Bohuon E J R , Ramsay L D , Craft J A , Arthur A E , Marshall D F , Lydiate D J , Kearsey M J 
Published: April 2021

Abstract
A population of 150 doubled haploid lines of rapid cycling Brassica oleracea, derived from an F1 from a var. alboglabra × var. italica cross, was scored for flowering time in two trials. Using information on 82 mapped molecular markers, spread evenly across the nine linkage groups, QTL were identified at six locations; one each on linkage groups O2 and O3 and two each on linkage groups O5 and O9. In total, these QTL explained 58 and 93% of the genetical variation in the two trials. Three of these QTL, on linkage groups O2, O3, and O9, were situated in regions showing considerable homology both with each other and with chromosome regions of B. nigra that have been shown to affect flowering time. These same regions are all homologous to a single tract of Arabidopsis chromosome 5, which contains a number of the flowering-related genes, one or more of which may be candidates for the QTL found in Brassica.
Arabidopsis TSO1 Regulates Directional Processes in Cells During Floral Organogenesis
Authors: Hauser Bernard A , Villanueva Jacinto M , Gasser Charles S 
Published: April 2021

Abstract
Flowers of the previously described Arabidopsis tso1-1 mutant had aberrant, highly reduced organs in place of petals, stamens, and carpels. Cells of tso1-1 flowers had division defects, including failure in cytokinesis, partial cell wall formation, and elevated nuclear DNA content. We describe here two new tso1 alleles (tso1-3 and tso1-4), which caused defects in ovule development, but had little effect on gross floral morphology. Early ovule development occurred normally in tso1-3 and tso1-4, but the shapes and alignments of integument cells became increasingly more disordered as development progressed. tso1-3 ovules usually lacked embryo sacs due to a failure to form megaspore mother cells. The cell division defects described for the strong tso1-1 mutant were rarely observed in tso1-3 ovules. The aberrations in tso1-3 mutants primarily resulted from a failure in directional expansion of cells and/or coordination of this process among adjacent cells. Effects of tso1-3 appeared to be independent of effects of other ovule development mutations, with the exception of leunig, which exhibited a synergistic interaction. The data are consistent with TSO1 acting in processes governing directional movement of cellular components, indicating a likely role for TSO1 in cytoskeletal function.
Statistical Analysis of Half-Tetrads
Authors: Zhao Hongyu , Speed Terence P 
Published: April 2021

Abstract
Half-tetrads, where two meiotic products from a single meiosis are recovered together, arise in different forms in a variety of organisms. Closely related to ordered tetrads, half-tetrads yield information on chromatid interference, chiasma interference, and centromere positions. In this article, for different half-tetrad types and different marker configurations, we derive the relations between multilocus half-tetrad probabilities and multilocus ordered tetrad probabilities. These relations are used to obtain equality and inequality constraints among multilocus half-tetrad probabilities that are imposed by the assumption of no chromatid interference. We illustrate how to apply these results to study chiasma interference and to map centromeres using multilocus half-tetrad data.
The Saccharomyces cerevisiae RAD9, RAD17, RAD24 and MEC3 Genes Are Required for Tolerating Irreparable, Ultraviolet-Induced DNA Damage
Authors: Paulovich A G , Armour C D , Hartwell L H 
Published: April 2021

Abstract
In wild-type Saccharomyces cerevisiae, a checkpoint slows the rate of progression of an ongoing S phase in response to exposure to a DNA-alkylating agent. Mutations that eliminate S phase regulation also confer sensitivity to alkylating agents, leading us to suggest that, by regulating the S phase rate, cells are either better able to repair or better able to replicate damaged DNA. In this study, we determine the effects of mutations that impair S phase regulation on the ability of excision repair-defective cells to replicate irreparably UV-damaged DNA. We assay survival after UV irradiation, as well as the genetic consequences of replicating a damaged template, namely mutation and sister chromatid exchange induction. We find that RAD9, RAD17, RAD24, and MEC3 are required for UV-induced (although not spontaneous) mutagenesis, and that RAD9 and RAD17 (but not REV3, RAD24, and MEC3) are required for maximal induction of replication-dependent sister chromatid exchange. Therefore, checkpoint genes not only control cell cycle progression in response to damage, but also play a role in accommodating DNA damage during replication.
Sex and the Evolution of Intrahost Competition in RNA Virus φ6
Authors: Turner Paul E , Chao Lin 
Published: April 2021

Abstract
Sex allows beneficial mutations that occur in separate lineages to be fixed in the same genome. For this reason, the Fisher-Muller model predicts that adaptation to the environment is more rapid in a large sexual population than in an equally large asexual population. Sexual reproduction occurs in populations of the RNA virus φ6 when multiple bacteriophages coinfect the same host cell. Here, we tested the model's predictions by determining whether sex favors more rapid adaptation of φ6 to a bacterial host, Pseudomonas phaseolicola. Replicate populations of φ6 were allowed to evolve in either the presence or absence of sex for 250 generations. All experimental populations showed a significant increase in fitness relative to the ancestor, but sex did not increase the rate of adaptation. Rather, we found that the sexual and asexual treatments also differ because intense intrahost competition between viruses occurs during coinfection. Results showed that the derived sexual viruses were selectively favored only when coinfection is common, indicating that within-host competition detracts from the ability of viruses to exploit the host. Thus, sex was not advantageous because the cost created by intrahost competition was too strong. Our findings indicate that high levels of coinfection exceed an optimum where sex may be beneficial to populations of φ6, and suggest that genetic conflicts can evolve in RNA viruses.
The Schizosaccharomyces pombe cho1+ Gene Encodes a Phospholipid Methyltransferase
Authors: Kanipes Margaret I , Hill John E , Henry Susan A 
Published: April 2021

Abstract
The isolation of mutants of Schizosaccharomyces pombe defective in the synthesis of phosphatidylcholine via the methylation of phosphatidylethanolamine is reported. These mutants are choline auxotrophs and fall into two unlinked complementation groups, cho1 and cho2. We also report the analysis of the cho1+ gene, the first structural gene encoding a phospholipid biosynthetic enzyme from S. pombe to be cloned and characterized. The cho1+ gene disruption mutant (cho1Δ) is viable if choline is supplied and resembles the cho1 mutants isolated after mutagenesis. Sequence analysis of the cho1+ gene indicates that it encodes a protein closely related to phospholipid methyltransferases from Saccharomyces cerevisiae and rat. Phospholipid methyltransferases encoded by a rat liver cDNA and the S. cerevisiae OPI3 gene are both able to complement the choline auxotrophy of the S. pombe cho1 mutants. These results suggest that both the structure and function of the phospholipid N-methyltransferases are broadly conserved among eukaryotic organisms.
Histone Deacetylase Homologs Regulate Epigenetic Inheritance of Transcriptional Silencing and Chromosome Segregation in Fission Yeast
Authors: Grewal Shiv I S , Bonaduce Michael J , Klar Amar J S 
Published: April 2021

Abstract
Position-effect control at the silent mat2-mat3 interval and at centromeres and telomeres in fission yeast is suggested to be mediated through the assembly of heterochromatin-like structures. Therefore, trans-acting genes that affect silencing may encode either chromatin proteins, factors that modify them, or factors that affect chromatin assembly. Here, we report the identification of an essential gene, clr6 (c ryptic loci r egulator), which encodes a putative histone deacetylase that when mutated affects epigenetically maintained repression at the mat2-mat3 region and at centromeres and reduces the fidelity of chromosome segregation. Furthermore, we show that the Clr3 protein, when mutated, alleviates recombination block at mat region as well as silencing at donor loci and at centromeres and telomeres, also shares strong homology to known histone deacetylases. Genetic analyses indicate that silencing might be regulated by at least two overlapping histone deacetylase activities. We also found that transient inhibition of histone deacetylase activity by trichostatin A results in the increased missegregation of chromosomes in subsequent generations and, remarkably, alters the imprint at the mat locus, causing the heritable conversion of the repressed epigenetic state to the expressed state. This work supports the model that the level of histone deacetylation has a role in the assembly of repressive heterochromatin and provides insight into the mechanism of epigenetic inheritance.
Expression and Properties of Wild-Type and Mutant Forms of the Drosophila Sex Comb on Midleg (SCM) Repressor Protein
Authors: Bornemann Douglas , Miller Ellen , Simon Jeffrey 
Published: April 2021

Abstract
The Sex comb on midleg (Scm) gene encodes a transcriptional repressor of the Polycomb group (PcG). Here we show that SCM protein is nuclear and that its expression is widespread during fly development. SCM protein contains a C-terminal domain, termed the SPM domain, which mediates protein-protein interactions. The biochemical function of another domain consisting of two 100-amino-acid-long repeats, termed “mbt” repeats, is unknown. We have determined the molecular lesions of nine Scm mutant alleles, which identify functional requirements for specific domains. The Scm alleles were tested for genetic interactions with mutations in other PcG genes. Intriguingly, three hypomorphic Scm mutations, which map within an mbt repeat, interact with PcG mutations more strongly than do Scm null alleles. The strongest interactions produce partial synthetic lethality that affects doubly heterozygous females more severely than males. We show that mbt repeat alleles produce stable SCM proteins that associate with normal sites in polytene chromosomes. We also analyzed progeny from Scm mutant germline clones to compare the effects of an mbt repeat mutation during embryonic vs. pupal development. We suggest that the mbt repeat alleles produce altered SCM proteins that incorporate into and impair function of PcG protein complexes.
Evidence for 3′ Untranslated Region-Dependent Autoregulation of the Drosophila Gene Encoding the Neuronal Nuclear RNA-Binding Protein ELAV
Authors: Samson Marie-Laure 
Published: April 2021

Abstract
The Drosophila locus embryonic lethal abnormal visual system (elav) encodes a nuclear RNA-binding protein essential for normal neuronal differentiation and maintenance of neurons. ELAV is thought to play its role by binding to RNAs produced by other genes necessary for neuronal differentiation and consequently to affect their metabolism by an as yet unknown mechanism. ELAV structural homologues have been identified in a wide range of organisms, including humans, indicating an important conserved role for the protein. Analysis of elav germline transformants presented here shows that one copy of elav minigenes lacking a complete 3′ untranslated region (3′ UTR) rescues null mutations at elav, but that two copies are lethal. Additional in vivo experiments demonstrate that elav expression is regulated through the 3′ UTR of the gene and indicate that this level of regulation is dependent upon ELAV itself. Because ELAV is an RNA-binding protein, the simplest model to account for these findings is that ELAV binds to the 3′ UTR of its own RNA to autoregulate its expression. I discuss the implications of these results for normal elav function.
Multiple Origins of Cytologically Identical Chromosome Inversions in the Anopheles gambiae Complex
Authors: Caccone Adalgisa , Min Gi-Sik , Powell Jeffrey R 
Published: April 2021

Abstract
For more than 60 years, evolutionary cytogeneticists have been using naturally occurring chromosomal inversions to infer phylogenetic histories, especially in insects with polytene chromosomes. The validity of this method is predicated on the assumption that inversions arise only once in the history of a lineage, so that sharing a particular inversion implies shared common ancestry. This assumption of monophyly has been generally validated by independent data. We present the first clear evidence that naturally occurring inversions, identical at the level of light microscopic examination of polytene chromosomes, may not always be monophyletic. The evidence comes from DNA sequence analyses of regions within or very near the breakpoints of an inversion called the 2La that is found in the Anopheles gambiae complex. Two species, A. merus and A. arabiensis, which are fixed for the “same” inversion, do not cluster with each other in a phylogenetic analysis of the DNA sequences within the 2La. Rather, A. merus 2La is most closely related to strains of A. gambiae homozygous for the 2L+. A. gambiae and A. merus are sister taxa, the immediate ancestor was evidently homozygous 2L+, and A. merus became fixed for an inversion cytologically identical to that in A. arabiensis. A. gambiae is polymorphic for 2La/2L+, and the 2La in this species is nearly identical at the DNA level to that in A. arabiensis, consistent with the growing evidence that introgression has or is occurring between these two most important vectors of malaria in the world. The parallel evolution of the “same” inversion may be promoted by the presence of selectively important genes within the breakpoints.
Genetic Variation and Phylogeography of Central Asian and Other House Mice, Including a Major New Mitochondrial Lineage in Yemen
Authors: Prager Ellen M , Orrego Cristián , Sage Richard D 
Published: April 2021

Abstract
The mitochondrial DNA (mtDNA) control region and flanking tRNAs were sequenced from 76 mice collected at 60 localities extending from Egypt through Turkey, Yemen, Iran, Afghanistan, Pakistan, and Nepal to eastern Asia. Segments of the Y chromosome and of a processed p53 pseudogene (ψp53) were amplified from many of these mice and from others collected elsewhere in Eurasia and North Africa. The 251 mtDNA types, including 54 new ones reported here, now identified from commensal house mice (Mus musculus group) by sequencing this segment can be organized into four major lineages—domesticus, musculus, castaneus, and a new lineage found in Yemen. Evolutionary tree analysis suggested the domesticus mtDNAs as the sister group to the other three commensal mtDNA lineages and the Yemeni mtDNAs as the next oldest lineage. Using this tree and the phylogeographic approach, we derived a new model for the origin and radiation of commensal house mice whose main features are an origin in west-central Asia (within the present-day range of M. domesticus) and the sequential spreading of mice first to the southern Arabian Peninsula, thence eastward and northward into south-central Asia, and later from south-central Asia to north-central Asia (and thence into most of northern Eurasia) and to southeastern Asia. Y chromosomes with and without an 18-bp deletion in the Zfy-2 gene were detected among mice from Iran and Afghanistan, while only undeleted Ys were found in Turkey, Yemen, Pakistan, and Nepal. Polymorphism for the presence of a ψp53 was observed in Georgia, Iran, Turkmenistan, Afghanistan, and Pakistan. Sequencing of a 128-bp ψp53 segment from 79 commensal mice revealed 12 variable sites and implicated ≥14 alleles. The allele that appeared to be phylogenetically ancestral was widespread, and the greatest diversity was observed in Turkey, Afghanistan, Pakistan, and Nepal. Two mice provided evidence for a second ψp53 locus in some commensal populations.
A High-Resolution Linkage Map of the Citrus Tristeza Virus Resistance Gene Region in Poncirus trifoliata (L.) Raf.
Authors: Fang D Q , Federici C T , Roose M L 
Published: April 2021

AbstractResistance to citrus tristeza virus (CTV) was evaluated in 554 progeny of 10 populations derived from Poncirus trifoliata. A dominant gene (Ctv) controlled CTV resistance in P. trifoliata. Twenty-one dominant PCR-based DNA markers were identified as linked to Ctv by bulked segregant analysis. Of the 11 closest markers to Ctv, only 2 segregated in all populations. Ten of these markers were cloned and sequenced, and codominant RFLP markers were developed. Seven RFLP markers were then evaluated in 10 populations. Marker orders were consistent in all linkage maps based on data of single populations or on combined data of populations with similar segregation patterns. In a consensus map, the six closest marker loci spanned 5.3 cM of the Ctv region. Z16 cosegregated with Ctv. C19 and AD08 flanked Ctv at distances of 0.5 and 0.8 cM, respectively. These 3 markers were present as single copies in the Poncirus genome, and could be used directly for bacterial artificial chromosome library screening to initiate a walk toward Ctv. BLAST searches of the GenBank database revealed high sequence similarities between 2 markers and known plant disease resistance genes, indicating that a resistance gene cluster exists in the Ctv region in P. trifoliata.