bluuebunny/crossref_metadata_2025_split huggingface dataset:
The incomplete natural history of mitochondria
Authors: Ballard J. William O. , Whitlock Michael C. 
Published: December 2004

AbstractMitochondrial DNA (mtDNA) has been used to study molecular ecology and phylogeography for 25 years. Much important information has been gained in this way, but it is time to reflect on the biology of the mitochondrion itself and consider opportunities for evolutionary studies of the organelle itself and its ecology, biochemistry and physiology. This review has four sections. First, we review aspects of the natural history of mitochondria and their DNA to show that it is a unique molecule with specific characteristics that differ from nuclear DNA. We do not attempt to cover the plethora of differences between mitochondrial and nuclear DNA; rather we spotlight differences that can cause significant bias when inferring demographic properties of populations and/or the evolutionary history of species. We focus on recombination, effective population size and mutation rate. Second, we explore some of the difficulties in interpreting phylogeographical data from mtDNA data alone and suggest a broader use of multiple nuclear markers. We argue that mtDNA is not a sufficient marker for phylogeographical studies if the focus of the investigation is the species and not the organelle. We focus on the potential bias caused by introgression. Third, we show that it is not safe to assumea priorithat mtDNA evolves as a strictly neutral marker because both direct and indirect selection influence mitochondria. We outline some of the statistical tests of neutrality that can, and should, be applied to mtDNA sequence data prior to making any global statements concerning the history of the organism. We conclude with a critical examination of the neglected biology of mitochondria and point out several surprising gaps in the state of our knowledge about this important organelle. Here we limelight mitochondrial ecology, sexually antagonistic selection, life‐history evolution including ageing and disease, and the evolution of mitochondrial inheritance.
Spatial structure and genetic diversity of two tropical tree species with contrasting breeding systems and different ploidy levels
Authors: Ng Kevin K. S. , Lee S. L. , Koh C. L. 
Published: December 2004

AbstractAnalyses of the spatial distribution pattern, spatial genetic structure and of genetic diversity were carried out in two tropical tree species with contrasting breeding systems and different ploidy levels using a 50‐ha demographic plot in a lowland dipterocarp forest in Peninsular Malaysia. Shorea leprosula is a diploid and predominantly outcrossed species, whereas S. ovalis ssp. sericea is an autotetraploid species with apomictic mode of reproduction. Genetic diversity parameters estimated for S. leprosula using microsatellite were consistently higher than using allozyme. In comparisons with S. leprosula and other tropical tree species, S. ovalis ssp. sericea also displayed relatively high levels of genetic diversity. This might be explained by the lower pressure of genetic drift due to tetrasomic inheritance, and for autotetraploids each locus can accommodate up to four different alleles and this allows maintenance of more alleles at individual loci. The observed high levels of genetic diversity in S. ovalis ssp. sericea can also be due to a random retention of more heterogeneous individuals in the past, and the apomictic mode of reproduction might be an evolutionary strategy, which allows the species to maintain high levels of genetic diversity. The spatial distribution pattern analyses of both species showed significant levels of aggregation at small and medium but random distribution at the big diameter‐class. The decrease in magnitude of spatial aggregation from small‐ to large‐diameter classes might be due to compensatory mortality during recruitment and survival under competitive thinning process. Spatial genetic structure analyses for both species revealed significant spatial genetic structure for short distances in all the three diameter‐classes. The magnitude of spatial genetic structure in both species was observed to be decreasing from smaller‐ to larger‐diameter classes. The high spatial genetic structuring observed in S. ovalis ssp. sericea at the small‐diameter class is due primarily to limited seed dispersal and apomictic mode of reproduction. The similar observation in S. leprosula, however, can be explained by limited seed and pollen dispersal, which supports further the fact that the species is pollinated by weak fliers, mainly of Thrips and Megalurothrips in the lowland dipterocarp forest.
Moment estimation of population diversity and genetic distance from data on recessive markers*
Authors: Hill W. G. , Weir B. S. 
Published: December 2004

AbstractA moment‐based method for estimating a measure of population diversity, θ or Wright's FST, is given for dominant markers such as amplified fragment length polymorphisms (AFLPs) or RAPDs in noninbred populations. Basic assumptions are that there is random mating, Hardy–Weinberg equilibrium, linkage equilibrium, no mutation from common ancestor and equally distant populations. It is based on the variances between and within populations of genotype frequencies, whereas previously moment methods for dominant markers have been indirect in that they have been based on first estimating allele frequencies and then using the variances of those frequencies. The use of genotype frequencies directly appears to be more robust. Approximate sampling errors of the estimates are given. Methods are extended to estimate genetic distances and their sampling errors. The AFLP data from samples of breeds of pig are used for illustration.
Two distinct regions on the surface of an RNA‐binding domain are crucial for RNase E function
Authors: Diwa Alexis A. , Jiang Xunqing , Schapira Matthieu , Belasco Joel G. 
Published: December 2004

SummaryDespite its importance for RNA processing and degradation in Escherichia coli, little is known about the structure of RNase E or its mechanism of action. We have modelled the three‐dimensional structure of an essential amino‐terminal domain of RNase E on the basis of its sequence homology to the S1 family of RNA‐binding domains. Each of the five surface‐exposed aromatic residues and most of the 14 basic residues of this RNase E domain were replaced with alanine to determine their importance for RNase E function. All the surface residues essential for cell growth and feedback regulation of RNase E synthesis mapped to one end of the domain. In vitro assays indicate that these essential residues fall into two functionally distinct groups that form discrete clusters on opposite faces of the S1 domain. One group, comprising Phe‐57, Phe‐67 and Tyr‐112, is of general importance for the ribonuclease activity of RNase E, whereas the other group, comprising Lys‐37 and Tyr‐60, is entirely dispensable for catalytic activity in vitro. The side‐chains of two residues previously identified as sites of temperature‐sensitive mutations lie buried directly beneath the surface region defined by Phe‐57, Phe‐67 and Tyr‐112, which probably enhances RNase E activity by making a crucial contribution to the binding of substrate RNAs. In contrast to the S1 domain, an arginine‐rich RNA‐binding domain in the carboxyl half of RNase E appears to have a more peripheral role in RNase E function, as it is not required for feedback regulation, cell growth or ribonuclease activity.
Aminoacyl‐tRNA synthesis in archaea: different but not unique
Authors: Prætorius‐Ibba Mette , Ibba Michael 
Published: December 2004

SummaryAccurate aminoacyl‐tRNA synthesis is essential for correct translation of the genetic code in all organisms. Whereas many aspects of this process are conserved, others display a surprisingly high level of divergence from the canonical Escherichia coli model system. These differences are most pronounced in archaea where novel mechanisms have recently been described for aminoacylating tRNAs with asparagine, cysteine, glutamine and lysine. Whereas these mechanisms were initially assumed to be uniquely archaeal, both the alternative asparagine and lysine pathways have subsequently been demonstrated in numerous bacteria. Similarly, studies of the means by which archaea insert the rare amino acid selenocysteine in response to UGA stop codons have helped provide a better understanding of both archaeal and eukaryal selenoprotein synthesis. Most recently a new co‐translationally inserted amino acid, pyrrolysine, has been found in archaea although again there is some suggestion that it may also be present in bacteria. Thus, whereas archaea contain a preponderance of non‐canonical aminoacyl‐tRNA synthesis systems most are also found elsewhere albeit less frequently.
Coupling gene expression and multicellular morphogenesis during fruiting body formation in Myxococcus xanthus
Authors: Søgaard‐Andersen Lotte , Overgaard Martin , Lobedanz Sune , Ellehauge Eva , Jelsbak Lars , Rasmussen Anders Aa. 
Published: December 2004

SummaryA recurring theme in morphogenesis is the coupling of the expression of genes that drive morphogenesis and the morphogenetic process per se. This coupling ensures that gene expression and morphogenesis are carried out in synchrony. Morphogenesis of the spore‐filled fruiting bodies in Myxococcus xanthus illustrates this coupling in the construction of a multicellular structure. Fruiting body formation involves two stages: aggregation of cells into mounds and the position‐specific sporulation of cells that have accumulated inside mounds. Developmental gene expression propels these two processes. In addition, gene expression in individual cells is adjusted according to their spatial position. Progress in the understanding of the cell surface‐associated C‐signal is beginning to reveal the framework of an intercellular signalling system that allows the coupling of gene expression and multicellular morphogenesis. Accumulation of the C‐signal is tightly regulated and involves transcriptional activation of the csgA gene and proteolysis of the full‐length CsgA protein to produce the shorter cell surface‐associated 17 kDa C‐signal protein. The C‐signal induces aggregation, sporulation and developmental gene expression at specific thresholds. The ordered increase in C‐signalling levels, in combination with the specific thresholds, allows the C‐signal to induce these three processes in the correct temporal order. The contact‐dependent C‐signal transmission mechanism, in turn, guarantees that C‐signalling levels reflect the spatial position of individual cells relative to other cells and, thus, allows the cells to decode their spatial position during morphogenesis. By this mechanism, individual cells can tailor their gene expression profile to one that matches their spatial position. In this scheme, the molecular device that keeps gene expression in individual cells in register with morphogenesis is the C‐signalling system, and the morphological structure, which is assessed, is the spatial position of individual cells relative to that of other cells.
C‐terminal domain mutations in ClpX uncouple substrate binding from an engagement step required for unfolding
Authors: Joshi Shilpa A. , Baker Tania A. , Sauer Robert T. 
Published: December 2004

SummaryClpX mediates ATP‐dependent denaturation of specific target proteins and disassembly of protein complexes. Like other AAA + family members, ClpX contains an αβ ATPase domain and an α‐helical C‐terminal domain. ClpX proteins with mutations in the C‐terminal domain were constructed and screened for disassembly activity in vivo. Seven mutant enzymes with defective phenotypes were purified and characterized. Three of these proteins (L381K, D382K and Y385A) had low activity in disassembly or unfolding assays in vitro. In contrast to wild‐type ClpX, substrate binding to these mutants inhibited ATP hydrolysis instead of increasing it. These mutants appear to be defective in a reaction step that engages bound substrate proteins and is required both for enhancement of ATP hydrolysis and for unfolding/disassembly. Some of these side chains form part of the interface between the C‐terminal domain of one ClpX subunit and the ATPase domain of an adjacent subunit in the hexamer and appear to be required for communication between adjacent nucleotide binding sites.
Citrobacter rodentium translocated intimin receptor (Tir) is an essential virulence factor needed for actin condensation, intestinal colonization and colonic hyperplasia in mice
Authors: Deng Wanyin , Vallance Bruce A. , Li Yuling , Puente Jose L. , Finlay B. Brett 
Published: December 2004

Summary Citrobacter rodentium infection of mice serves as a relevant small animal model to study enterohaemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC) infections in man. Enteropathogenic E. coli and EHEC translocate Tir into the host cytoplasmic membrane, where it serves as the receptor for the bacterial adhesin intimin and plays a central role in actin condensation beneath the adherent bacterium. In this report, we examined the function of C. rodentium Tir both in vitro and in vivo. Similar to EPEC, C. rodentium Tir is tyrosine phosphorylated and is essential for actin condensation. Citrobacter Tir and EPEC Tir are functionally interchangeable and both require tyrosine phosphorylation to mediate actin rearrangements. In contrast, Citrobacter Tir supports actin nucleation in EHEC independent of tyrosine phosphorylation, while EHEC Tir cannot replace Citrobacter Tir for this function. This indicates that C. rodentium and EPEC use an actin nucleating mechanism different from EHEC. We also found that Tir is expressed and translocated into mouse enterocytes in vivo by C. rodentium during infections. This represents the first direct demonstration of a type III effector translocated in vivo into a natural host by any pathogen. In addition, we showed that Tir, but not its tyrosine phosphorylation, is essential for C. rodentium to colonize the large bowel and induce attaching/effacing (A/E) lesions and colonic hyperplasia in mice, and that both EPEC Tir and EHEC Tir can substitute for Citrobacter Tir for these activities in vivo. These results thus demonstrate that Tir is an essential virulence factor in this infection model. The data also show that the function of Tir tyrosine phosphorylation and its subsequent actin nucleating activity are not essential for C. rodentium colonization of the mouse gut nor for inducing A/E lesions and colonic hyperplasia, thereby uncoupling colonization and disease from actin condensation for this A/E pathogen.
Global gene expression in Escherichia coli biofilms
Authors: Schembri Mark A. , Kjærgaard Kristian , Klemm Per 
Published: December 2004

SummaryIt is now apparent that microorganisms undergo significant changes during the transition from planktonic to biofilm growth. These changes result in phenotypic adaptations that allow the formation of highly organized and structured sessile communities, which possess enhanced resistance to antimicrobial treatments and host immune defence responses. Escherichia coli has been used as a model organism to study the mechanisms of growth within adhered communities. In this study, we use DNA microarray technology to examine the global gene expression profile of E. coli during sessile growth compared with planktonic growth. Genes encoding proteins involved in adhesion (type 1 fimbriae) and, in particular, autoaggregation (Antigen 43) were highly expressed in the adhered population in a manner that is consistent with current models of sessile community development. Several novel gene clusters were induced upon the transition to biofilm growth, and these included genes expressed under oxygen‐limiting conditions, genes encoding (putative) transport proteins, putative oxidoreductases and genes associated with enhanced heavy metal resistance. Of particular interest was the observation that many of the genes altered in expression have no current defined function. These genes, as well as those induced by stresses relevant to biofilm growth such as oxygen and nutrient limitation, may be important factors that trigger enhanced resistance mechanisms of sessile communities to antibiotics and hydrodynamic shear forces.
Phosphorylation‐mediated regulation of heat shock response in Escherichia coli
Authors: Klein Gracjana , Dartigalongue Claire , Raina Satish 
Published: December 2004

Summary Escherichia coli has two heat shock regulons under the transcriptional control of Eσ32 and EσE RNA polymerases. These polymerases control the expression of genes, the products of which are needed for correct folding of proteins in the cytoplasm and the extracytoplasm respectively. In this study, we report that mutations in a tyrosine phosphatase‐encoding gene led to decreased activity of these heat shock regulons. The activity of the tyrosine phosphatase is presumably co‐ordinated with that of a cognate kinase. We show here that mutants deleted for the phosphatase‐encoding gene accumulate phosphorylated RpoH. We find that RpoH is phosphorylated at amino acid position 260, which is located in the conserved region 4.2, and that this phosphorylation event attenuates RpoH activity as a sigma factor. The rpoH Tyr‐260Ala mutation confers a temperature‐sensitive phenotype that leads to an altered heat shock response. Additionally, we show that the antisigma factor RseA is phosphorylated at the N‐terminally located Tyr‐38 and that this phosphorylation presumably alters its binding affinity towards σE.
A plasmid‐encoded nicotinamidase (PncA) is essential for infectivity of Borrelia burgdorferi in a mammalian host
Authors: Purser Joye E. , Lawrenz Matthew B. , Caimano Melissa J. , Howell Jerrilyn K. , Radolf Justin D. , Norris Steven J. 
Published: December 2004

Summary Borrelia burgdorferi, a spirochaete that causes Lyme borreliosis, contains 21 linear and circular plasmids thought to be important for survival in mammals or ticks. Our results demonstrate that the gene BBE22 encoding a nicotinamidase is capable of replacing the requirement for the 25 kb linear plasmid lp25 during mammalian infection. Transformation of B. burgdorferi lacking lp25 with a shuttle vector containing the lp25 gene BBE22 (pBBE22) restored infectivity in mice to a level comparable to that of wild‐type Borrelia. This complementation also restored the growth and host adaptation of lp25–B. burgdorferi in dialysis membrane chambers (DMCs) implanted in rats. A single Cys to Ala conversion at the putative active site of BBE22 abrogated the ability of pBBE22 to re‐establish infectivity or growth in DMCs. Additional Salmonella typhimurium complementation studies and enzymatic analysis demonstrated that the BBE22 gene product has nicotinamidase activity and is most probably required for the biosynthesis of NAD. These results indicate that some plasmid‐encoded products fulfil physiological functions required in the enzootic cycle of pathogenic Borrelia.
A novel sRNA component of the carbon storage regulatory system of Escherichia coli
Authors: Weilbacher Thomas , Suzuki Kazushi , Dubey Ashok K. , Wang Xin , Gudapaty Seshigirao , Morozov Igor , Baker Carol S. , Georgellis Dimitris , Babitzke Paul , Romeo Tony 
Published: December 2004

SummarySmall untranslated RNAs (sRNAs) perform a variety of important functions in bacteria. The 245 nucleotide sRNA of Escherichia coli, CsrC, was discovered using a genetic screen for factors that regulate glycogen biosynthesis. CsrC RNA binds multiple copies of CsrA, a protein that post‐transcriptionally regulates central carbon flux, biofilm formation and motility in E. coli. CsrC antagonizes the regulatory effects of CsrA, presumably by sequestering this protein. The discovery of CsrC is intriguing, in that a similar sRNA, CsrB, performs essentially the same function. Both sRNAs possess similar imperfect repeat sequences (18 in CsrB, nine in CsrC), primarily localized in the loops of predicted hairpins, which may serve as CsrA binding elements. Transcription of csrC increases as the culture approaches the stationary phase of growth and is indirectly activated by CsrA via the response regulator UvrY. Because CsrB and CsrC antagonize CsrA activity and depend on CsrA for their synthesis, a csrB null mutation causes a modest compensatory increase in CsrC levels and vice versa. Homologues of csrC are apparent in several Enterobacteriaceae. The regulatory and evolutionary implications of these findings are discussed.
Structure and genotypic plasticity of the Campylobacter fetus sap locus
Authors: Tu Zheng‐Chao , Wassenaar Trudy M. , Thompson Stuart A. , Blaser Martin J. 
Published: December 2004

SummaryThe Campylobacter fetus surface layer proteins (SLPs), encoded by five to nine sapA homologues, are major virulence factors. To characterize the sapA homologues further, a 65.9 kb C. fetus genomic region encompassing the sap locus from wild‐type strain 23D was completely sequenced and analysed; 44 predicted open reading frames (ORFs) were recognized. The 53.8 kb sap locus contained eight complete and one partial sapA homologues, varying from 2769 to 3879 bp, sharing conserved 553–2622 bp 5′ regions, with partial sharing of 5′ and 3′ non‐coding regions. All eight sapA homologues were expressed in Escherichia coli as antigenic proteins and reattached to the surface of SLP– strain 23B, indicating their conserved function. Analysis of the sap homologues indicated three phylogenetic groups. Promoter‐specific polymerase chain reactions (PCRs) and sapA homologue‐specific reverse transcription (RT)‐PCRs showed that the unique sapA promoter can potentially express all eight sapA homologues. Reciprocal DNA recombination based on the 5′ conserved regions can involve each of the eight sapA homologues, with frequencies from 10−1 to 10−3. Intragenic recombination between sapA7 and sapAp8, mediated by their conserved regions with a 10−1−10−2 frequency, allows the formation of new sap homologues. As divergent SLP C‐termini possess multiple antigenic sites, their reciprocal recombination behind the unique sap promoter leads to continuing antigenic variation.
The pH signalling transcription factor PacC controls virulence in the plant pathogen Fusarium oxysporum
Authors: Caracuel Zaira , Roncero M. Isabel G. , Espeso Eduardo A. , González‐Verdejo Clara I. , García‐Maceira Fe I. , Di Pietro Antonio 
Published: December 2004

SummaryGene expression in fungi by ambient pH is regulated via a conserved signalling cascade whose terminal component is the zinc finger transcription factor PacC/Rim1p. We have identified a pacC orthologue in the vascular wilt pathogen Fusarium oxysporum that binds the consensus 5′‐GCCAAG‐3′ sequence and is proteolytically processed in a similar way to PacC from Aspergillus nidulans. pacC transcript levels were elevated in F. oxysporum grown in alkaline conditions and almost undetectable at extreme acidic growth conditions. PacC+/– loss‐of‐function mutants displayed an acidity‐mimicking phenotype resulting in poor growth at alkaline pH, increased acid protease activity and higher transcript levels of acid‐expressed polygalacturonase genes. Reintroduction of a functional pacC copy into a pacC+/– mutant restored the  wild‐type phenotype. Conversely, F. oxysporum merodiploids carrying a dominant activating pacCc allele had increased pacC transcript and protein levels and displayed an alkalinity‐mimicking phenotype with reduced acid phosphatase and increased alkaline protease activities. PacC+/– mutants were more virulent than the wild‐type strain in root infection assays with tomato plants, whereas pacCc strains were significantly reduced in virulence. We propose that F. oxysporum PacC acts as a negative regulator of virulence to plants, possibly by preventing transcription of acid‐expressed genes important for infection.