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1.
Elife ; 112022 01 06.
Article in English | MEDLINE | ID: mdl-34989337

ABSTRACT

Y chromosomes across diverse species convergently evolve a gene-poor, heterochromatic organization enriched for duplicated genes, LTR retrotransposons, and satellite DNA. Sexual antagonism and a loss of recombination play major roles in the degeneration of young Y chromosomes. However, the processes shaping the evolution of mature, already degenerated Y chromosomes are less well-understood. Because Y chromosomes evolve rapidly, comparisons between closely related species are particularly useful. We generated de novo long-read assemblies complemented with cytological validation to reveal Y chromosome organization in three closely related species of the Drosophila simulans complex, which diverged only 250,000 years ago and share >98% sequence identity. We find these Y chromosomes are divergent in their organization and repetitive DNA composition and discover new Y-linked gene families whose evolution is driven by both positive selection and gene conversion. These Y chromosomes are also enriched for large deletions, suggesting that the repair of double-strand breaks on Y chromosomes may be biased toward microhomology-mediated end joining over canonical non-homologous end-joining. We propose that this repair mechanism contributes to the convergent evolution of Y chromosome organization across organisms.


Subject(s)
Chromosomes, Insect/genetics , Drosophila/genetics , Evolution, Molecular , Selection, Genetic , Y Chromosome/genetics , Animals , Drosophila melanogaster/genetics , Drosophila simulans/genetics , Species Specificity
2.
Front Genet ; 12: 669045, 2021.
Article in English | MEDLINE | ID: mdl-34249091

ABSTRACT

The three fruitfly species of the Drosophila simulans clade- D. simulans, D. mauritiana, and D. sechellia- have served as important models in speciation genetics for over 40 years. These species are reproductively isolated by geography, ecology, sexual signals, postmating-prezygotic interactions, and postzygotic genetic incompatibilities. All pairwise crosses between these species conform to Haldane's rule, producing fertile F1 hybrid females and sterile F1 hybrid males. The close phylogenetic proximity of the D. simulans clade species to the model organism, D. melanogaster, has empowered genetic analyses of their species differences, including reproductive incompatibilities. But perhaps no phenotype has been subject to more continuous and intensive genetic scrutiny than hybrid male sterility. Here we review the history, progress, and current state of our understanding of hybrid male sterility among the D. simulans clade species. Our aim is to integrate the available information from experimental and population genetics analyses bearing on the causes and consequences of hybrid male sterility. We highlight numerous conclusions that have emerged as well as issues that remain unresolved. We focus on the special role of sex chromosomes, the fine-scale genetic architecture of hybrid male sterility, and the history of gene flow between species. The biggest surprises to emerge from this work are that (i) genetic conflicts may be an important general force in the evolution of hybrid incompatibility, (ii) hybrid male sterility is polygenic with contributions of complex epistasis, and (iii) speciation, even among these geographically allopatric taxa, has involved the interplay of gene flow, negative selection, and positive selection. These three conclusions are marked departures from the classical views of speciation that emerged from the modern evolutionary synthesis.

3.
Genome Res ; 31(3): 380-396, 2021 03.
Article in English | MEDLINE | ID: mdl-33563718

ABSTRACT

The rapid evolution of repetitive DNA sequences, including satellite DNA, tandem duplications, and transposable elements, underlies phenotypic evolution and contributes to hybrid incompatibilities between species. However, repetitive genomic regions are fragmented and misassembled in most contemporary genome assemblies. We generated highly contiguous de novo reference genomes for the Drosophila simulans species complex (D. simulans, D. mauritiana, and D. sechellia), which speciated ∼250,000 yr ago. Our assemblies are comparable in contiguity and accuracy to the current D. melanogaster genome, allowing us to directly compare repetitive sequences between these four species. We find that at least 15% of the D. simulans complex species genomes fail to align uniquely to D. melanogaster owing to structural divergence-twice the number of single-nucleotide substitutions. We also find rapid turnover of satellite DNA and extensive structural divergence in heterochromatic regions, whereas the euchromatic gene content is mostly conserved. Despite the overall preservation of gene synteny, euchromatin in each species has been shaped by clade- and species-specific inversions, transposable elements, expansions and contractions of satellite and tRNA tandem arrays, and gene duplications. We also find rapid divergence among Y-linked genes, including copy number variation and recent gene duplications from autosomes. Our assemblies provide a valuable resource for studying genome evolution and its consequences for phenotypic evolution in these genetic model species.


Subject(s)
Drosophila simulans/classification , Drosophila simulans/genetics , Evolution, Molecular , Genome, Insect/genetics , Animals , DNA Copy Number Variations/genetics , DNA Transposable Elements/genetics , DNA, Satellite/genetics , Drosophila melanogaster/genetics , Female , Male
4.
PLoS Biol ; 18(3): e3000663, 2020 03.
Article in English | MEDLINE | ID: mdl-32203540

ABSTRACT

During in vitro fertilisation (IVF), pharmacological activation of the murine X chromosome-encoded receptor proteins Toll-like receptor (TLR) 7 and TLR8 reportedly results in male-biased litters by selectively disrupting the motility of X-bearing sperm cells. Thus-in the context of agonist treatment during IVF-these receptors act as 'suicidal' segregation distorters that impair their own transmission to the next generation. Such behaviour would, from an evolutionary perspective, be strongly selected against if present during natural fertilisation. Consequently, TLR7/8 biology in vivo must differ significantly from this in vitro situation to allow these genes to persist in the genome. Here, we use our current understanding of male germ cell biology and TLR function as a starting point to explore the mechanistic and evolutionary aspects of this apparent paradox.


Subject(s)
Spermatozoa/physiology , Toll-Like Receptors/metabolism , X Chromosome , Animals , Biological Evolution , Humans , Male , RNA Transport , Sex Ratio , Spermatogenesis , Spermatozoa/cytology , Spermatozoa/metabolism , Toll-Like Receptors/genetics
5.
Integr Comp Biol ; 59(4): 890-899, 2019 10 01.
Article in English | MEDLINE | ID: mdl-31173136

ABSTRACT

Strict maternal transmission of mitochondrial DNA (mtDNA) is hypothesized to permit the accumulation of mitochondrial variants that are deleterious to males but not females, a phenomenon called mother's curse. However, direct evidence that mtDNA mutations exhibit such sexually antagonistic fitness effects is sparse. Male-specific mutational effects can occur when the physiological requirements of the mitochondria differ between the sexes. Such male-specific effects could potentially occur if sex-specific cell types or tissues have energy requirements that are differentially impacted by mutations affecting energy metabolism. Here we summarize findings from a model mitochondrial-nuclear incompatibility in the fruit fly Drosophila that demonstrates sex-biased effects, but with deleterious effects that are generally larger in females. We present new results showing that the mitochondrial-nuclear incompatibility does negatively affect male fertility, but only when males are developed at high temperatures. The temperature-dependent male sterility can be partially rescued by diet, suggesting an energetic basis. Finally, we discuss fruitful paths forward in understanding the physiological scope for sex-specific effects of mitochondrial mutations in the context of the recent discovery that many aspects of metabolism are sexually dimorphic and downstream of sex-determination pathways in Drosophila. A key parameter of these models that remains to be quantified is the fraction of mitochondrial mutations with truly male-limited fitness effects across extrinsic and intrinsic environments. Given the energy demands of reproduction in females, only a small fraction of the mitochondrial mutational spectrum may have the potential to contribute to mother's curse in natural populations.


Subject(s)
Biological Evolution , Cell Nucleus/genetics , Drosophila melanogaster/physiology , Maternal Inheritance/genetics , Mitochondria/genetics , Mutation/genetics , Temperature , Animals , DNA, Mitochondrial/genetics , Drosophila melanogaster/genetics , Female , Male , Reproduction/genetics , Selection, Genetic
6.
Elife ; 72018 12 13.
Article in English | MEDLINE | ID: mdl-30543325

ABSTRACT

During speciation, sex chromosomes often accumulate interspecific genetic incompatibilities faster than the rest of the genome. The drive theory posits that sex chromosomes are susceptible to recurrent bouts of meiotic drive and suppression, causing the evolutionary build-up of divergent cryptic sex-linked drive systems and, incidentally, genetic incompatibilities. To assess the role of drive during speciation, we combine high-resolution genetic mapping of X-linked hybrid male sterility with population genomics analyses of divergence and recent gene flow between the fruitfly species, Drosophila mauritiana and D. simulans. Our findings reveal a high density of genetic incompatibilities and a corresponding dearth of gene flow on the X chromosome. Surprisingly, we find that a known drive element recently migrated between species and, rather than contributing to interspecific divergence, caused a strong reduction in local sequence divergence, undermining the evolution of hybrid sterility. Gene flow can therefore mediate the effects of selfish genetic elements during speciation.


Subject(s)
Biological Evolution , Genetic Speciation , X Chromosome/genetics , Y Chromosome/genetics , Animals , Drosophila/genetics , Drosophila simulans/genetics , Gene Flow , Infertility, Male/genetics , Male , Meiosis/genetics , Species Specificity
7.
PLoS Biol ; 16(10): e3000036, 2018 10.
Article in English | MEDLINE | ID: mdl-30376563

ABSTRACT

Organisms are locked in an eternal struggle with parasitic DNA sequences that live inside their genomes and wreak havoc on their host's chromosomes as they spread through populations. To combat these parasites, host species have evolved elaborate mechanisms of resistance that suppress their activity. A new study in Drosophila indicates that, prior to the acquisition of resistance, individuals can vary in their ability to tolerate the activity of these genomic parasites, ignoring or repairing the damage they induce. This tolerance results from variation at genes involved in germline development and DNA damage checkpoints and suggests that these highly conserved cellular processes may be influenced by current and historical intragenomic parasite loads.


Subject(s)
Drosophila , Parasites , Animals , Female , Germ Cells , Host-Parasite Interactions , Humans , Immune Tolerance
8.
Dev Cell ; 46(3): 251-253, 2018 08 06.
Article in English | MEDLINE | ID: mdl-30086297

ABSTRACT

Species with chromosomal sex determination are susceptible to an evolutionary tug-of-war over sex chromosome segregation. RNA silencing has been proposed to play a role in this intragenomic conflict. Reporting in Developmental Cell, Lin et al. (2018) demonstrate that RNA interference is key to this conflict as a genome defender.


Subject(s)
Chromosome Segregation , RNA Interference , Biological Evolution
9.
Integr Comp Biol ; 58(3): 591-603, 2018 09 01.
Article in English | MEDLINE | ID: mdl-29945242

ABSTRACT

Physiological responses to short-term environmental stressors, such as infection, can have long-term consequences for fitness, particularly if the responses are inappropriate or nutrient resources are limited. Genetic variation affecting energy acquisition, storage, and usage can limit cellular energy availability and may influence resource-allocation tradeoffs even when environmental nutrients are plentiful. Here, we utilized Drosophila mitochondrial-nuclear genotypes to test whether disrupted mitochondrial function interferes with nutrient-sensing pathways, and whether this disruption has consequences for tradeoffs between immunity and fecundity. We found that an energetically-compromised genotype was relatively resistant to rapamycin-a drug that targets nutrient-sensing pathways and mimics resource limitation. Dietary resource limitation decreased survival of energetically-compromised flies. Furthermore, survival of infection with a natural pathogen was decreased in this genotype, and females of this genotype experienced immunity-fecundity tradeoffs that were not evident in genotypic controls with normal energy metabolism. Together, these results suggest that this genotype may have little excess energetic capacity and fewer cellular nutrients, even when environmental nutrients are not limiting. Genetic variation in energy metabolism may therefore act to limit the resources available for allocation to life-history traits in ways that generate tradeoffs even when environmental resources are not limiting.


Subject(s)
Drosophila melanogaster/physiology , Drosophila simulans/physiology , Genotype , Life History Traits , Mitochondria/physiology , Animals , Drosophila melanogaster/genetics , Drosophila simulans/genetics , Female , Fertility , Hybridization, Genetic , Immunity, Innate , Male , Nutritional Status , Oxidative Phosphorylation , Stress, Physiological
10.
PLoS Biol ; 14(7): e1002499, 2016 07.
Article in English | MEDLINE | ID: mdl-27404402

ABSTRACT

The evolution of heteromorphic sex chromosomes has repeatedly resulted in the evolution of sex chromosome-specific forms of regulation, including sex chromosome dosage compensation in the soma and meiotic sex chromosome inactivation in the germline. In the male germline of Drosophila melanogaster, a novel but poorly understood form of sex chromosome-specific transcriptional regulation occurs that is distinct from canonical sex chromosome dosage compensation or meiotic inactivation. Previous work shows that expression of reporter genes driven by testis-specific promoters is considerably lower-approximately 3-fold or more-for transgenes inserted into X chromosome versus autosome locations. Here we characterize this transcriptional suppression of X-linked genes in the male germline and its evolutionary consequences. Using transgenes and transpositions, we show that most endogenous X-linked genes, not just testis-specific ones, are transcriptionally suppressed several-fold specifically in the Drosophila male germline. In wild-type testes, this sex chromosome-wide transcriptional suppression is generally undetectable, being effectively compensated by the gene-by-gene evolutionary recruitment of strong promoters on the X chromosome. We identify and experimentally validate a promoter element sequence motif that is enriched upstream of the transcription start sites of hundreds of testis-expressed genes; evolutionarily conserved across species; associated with strong gene expression levels in testes; and overrepresented on the X chromosome. These findings show that the expression of X-linked genes in the Drosophila testes reflects a balance between chromosome-wide epigenetic transcriptional suppression and long-term compensatory adaptation by sex-linked genes. Our results have broad implications for the evolution of gene expression in the Drosophila male germline and for genome evolution.


Subject(s)
Drosophila melanogaster/genetics , Transcription, Genetic , X Chromosome Inactivation , Animals , Base Sequence , Conserved Sequence , Drosophila Proteins/biosynthesis , Drosophila Proteins/genetics , Female , Genes, Essential , Genes, X-Linked , Germ Cells/metabolism , Male , Promoter Regions, Genetic , Testis/metabolism , X Chromosome
11.
Proc Natl Acad Sci U S A ; 113(15): 3915-7, 2016 Apr 12.
Article in English | MEDLINE | ID: mdl-27035999
12.
Genome Res ; 24(1): 84-95, 2014 Jan.
Article in English | MEDLINE | ID: mdl-24043293

ABSTRACT

Evolutionary changes in gene expression underlie many aspects of phenotypic diversity within and among species. Understanding the genetic basis for evolved changes in gene expression is therefore an important component of a comprehensive understanding of the genetic basis of phenotypic evolution. Using interspecific introgression hybrids, we examined the genetic basis for divergence in genome-wide patterns of gene expression between Drosophila simulans and Drosophila mauritiana. We find that cis-regulatory and trans-regulatory divergences differ significantly in patterns of genetic architecture and evolution. The effects of cis-regulatory divergence are approximately additive in heterozygotes, quantitatively different between males and females, and well predicted by expression differences between the two parental species. In contrast, the effects of trans-regulatory divergence are associated with largely dominant introgressed alleles, have similar effects in the two sexes, and generate expression levels in hybrids outside the range of expression in both parental species. Although the effects of introgressed trans-regulatory alleles are similar in males and females, expression levels of the genes they regulate are sexually dimorphic between the parental D. simulans and D. mauritiana strains, suggesting that pure-species genotypes carry unlinked modifier alleles that increase sexual dimorphism in expression. Our results suggest that independent effects of cis-regulatory substitutions in males and females may favor their role in the evolution of sexually dimorphic phenotypes, and that trans-regulatory divergence is an important source of regulatory incompatibilities.


Subject(s)
Drosophila/genetics , Evolution, Molecular , Gene Expression Regulation , Genome, Insect , Regulatory Elements, Transcriptional , Alleles , Animals , Biological Evolution , Female , Gene Expression Profiling , Hybridization, Genetic , Male , Models, Genetic , Organ Specificity , Sex Characteristics , Species Specificity
13.
G3 (Bethesda) ; 4(1): 1-10, 2014 Jan 10.
Article in English | MEDLINE | ID: mdl-24318925

ABSTRACT

Imprinting is well-documented in both plant and animal species. In Drosophila, the Y chromosome is differently modified when transmitted through the male and female germlines. Here, we report genome-wide gene expression effects resulting from reversed parent-of-origin of the X and Y chromosomes. We found that hundreds of genes are differentially expressed between adult male Drosophila melanogaster that differ in the maternal and paternal origin of the sex chromosomes. Many of the differentially regulated genes are expressed specifically in testis and midgut cells, suggesting that sex chromosome imprinting might globally impact gene expression in these tissues. In contrast, we observed much fewer Y-linked parent-of-origin effects on genome-wide gene expression in females carrying a Y chromosome, indicating that gene expression in females is less sensitive to sex chromosome parent-of-origin. Genes whose expression differs between females inheriting a maternal or paternal Y chromosome also show sex chromosome parent-of-origin effects in males, but the direction of the effects on gene expression (overexpression or underexpression) differ between the sexes. We suggest that passage of sex chromosome chromatin through male meiosis may be required for wild-type function in F1 progeny, whereas disruption of Y-chromosome function through passage in the female germline likely arises because the chromosome is not adapted to the female germline environment.


Subject(s)
Drosophila/genetics , Gene Expression Regulation , Genome , Genomic Imprinting , X Chromosome , Y Chromosome , Animals , Chromatin/metabolism , Female , Genotype , Intestinal Mucosa/metabolism , Male , Meiosis , Testis/metabolism , X Chromosome/genetics , X Chromosome/metabolism , Y Chromosome/genetics , Y Chromosome/metabolism
14.
PLoS Genet ; 9(1): e1003238, 2013.
Article in English | MEDLINE | ID: mdl-23382693

ABSTRACT

Mitochondrial transcription, translation, and respiration require interactions between genes encoded in two distinct genomes, generating the potential for mutations in nuclear and mitochondrial genomes to interact epistatically and cause incompatibilities that decrease fitness. Mitochondrial-nuclear epistasis for fitness has been documented within and between populations and species of diverse taxa, but rarely has the genetic or mechanistic basis of these mitochondrial-nuclear interactions been elucidated, limiting our understanding of which genes harbor variants causing mitochondrial-nuclear disruption and of the pathways and processes that are impacted by mitochondrial-nuclear coevolution. Here we identify an amino acid polymorphism in the Drosophila melanogaster nuclear-encoded mitochondrial tyrosyl-tRNA synthetase that interacts epistatically with a polymorphism in the D. simulans mitochondrial-encoded tRNA(Tyr) to significantly delay development, compromise bristle formation, and decrease fecundity. The incompatible genotype specifically decreases the activities of oxidative phosphorylation complexes I, III, and IV that contain mitochondrial-encoded subunits. Combined with the identity of the interacting alleles, this pattern indicates that mitochondrial protein translation is affected by this interaction. Our findings suggest that interactions between mitochondrial tRNAs and their nuclear-encoded tRNA synthetases may be targets of compensatory molecular evolution. Human mitochondrial diseases are often genetically complex and variable in penetrance, and the mitochondrial-nuclear interaction we document provides a plausible mechanism to explain this complexity.


Subject(s)
Amino Acyl-tRNA Synthetases , Drosophila , Oxidative Phosphorylation , RNA, Transfer , Amino Acids , Amino Acyl-tRNA Synthetases/genetics , Amino Acyl-tRNA Synthetases/metabolism , Animals , Cell Nucleus/genetics , Cell Nucleus/metabolism , Drosophila/genetics , Drosophila/growth & development , Drosophila/physiology , Epistasis, Genetic , Evolution, Molecular , Genetic Fitness , Humans , Mitochondria/genetics , Mitochondria/metabolism , Mitochondrial Diseases , Molecular Sequence Data , Polymorphism, Genetic , RNA, Transfer/genetics , Tyrosine-tRNA Ligase/metabolism
15.
Genome Biol Evol ; 4(10): 1007-16, 2012.
Article in English | MEDLINE | ID: mdl-22975718

ABSTRACT

Male-biased genes-those expressed at higher levels in males than in females-are underrepresented on the X chromosome of Drosophila melanogaster. Several evolutionary models have been posited to explain this so-called demasculinization of the X. Here, we show that the apparent paucity of male-biased genes on the X chromosome is attributable to global X-autosome differences in expression in Drosophila testes, owing to a lack of sex chromosome dosage compensation in the male germline, but not to any difference in the density of testis-specific or testis-biased genes on the X chromosome. First, using genome-wide gene expression data from 20 tissues, we find no evidence that genes with testis-specific expression are underrepresented on the X chromosome. Second, using contrasts in gene expression profiles among pairs of tissues, we recover a statistical underrepresentation of testis-biased genes on the X but find that the pattern largely disappears once we account for the lack of dosage compensation in the Drosophila male germline. Third, we find that computationally "demasculinizing" the autosomes is not sufficient to produce an expression profile similar to that of the X chromosome in the testes. Our findings thus show that the lack of sex chromosome dosage compensation in Drosophila testes can explain the apparent signal of demasculinization on the X, whereas evolutionary demasculinization of the X cannot explain its overall reduced expression in the testes.


Subject(s)
Drosophila melanogaster/genetics , Genes, X-Linked , Spermatozoa/metabolism , X Chromosome/genetics , Animals , Anopheles/genetics , Dosage Compensation, Genetic , Female , Gene Dosage , Gene Expression Profiling , Genes, Insect , Male , Sex Characteristics , Testis/metabolism , Transcription, Genetic
16.
PLoS Biol ; 9(8): e1001126, 2011 Aug.
Article in English | MEDLINE | ID: mdl-21857805

ABSTRACT

The evolution of heteromorphic sex chromosomes (e.g., XY in males or ZW in females) has repeatedly elicited the evolution of two kinds of chromosome-specific regulation: dosage compensation--the equalization of X chromosome gene expression in males and females--and meiotic sex chromosome inactivation (MSCI)--the transcriptional silencing and heterochromatinization of the X during meiosis in the male (or Z in the female) germline. How the X chromosome is regulated in the Drosophila melanogaster male germline is unclear. Here we report three new findings concerning gene expression from the X in Drosophila testes. First, X chromosome-wide dosage compensation appears to be absent from most of the Drosophila male germline. Second, microarray analysis provides no evidence for X chromosome-specific inactivation during meiosis. Third, we confirm the previous discovery that the expression of transgene reporters driven by autosomal spermatogenesis-specific promoters is strongly reduced when inserted on the X chromosome versus the autosomes; but we show that this chromosomal difference in expression is established in premeiotic cells and persists in meiotic cells. The magnitude of the X-autosome difference in transgene expression cannot be explained by the absence of dosage compensation, suggesting that a previously unrecognized mechanism limits expression from the X during spermatogenesis in Drosophila. These findings help to resolve several previously conflicting reports and have implications for patterns of genome evolution and speciation in Drosophila.


Subject(s)
Dosage Compensation, Genetic/genetics , Drosophila/genetics , Meiosis/genetics , Sex Chromosomes/genetics , Animals , Female , Germ Cells/metabolism , Male , Spermatogenesis/genetics , Testis/metabolism , X Chromosome Inactivation/genetics
17.
Evolution ; 64(12): 3364-79, 2010 Dec.
Article in English | MEDLINE | ID: mdl-20624176

ABSTRACT

Efficient mitochondrial function requires physical interactions between the proteins encoded by the mitochondrial and nuclear genomes. Coevolution between these genomes may result in the accumulation of incompatibilities between divergent lineages. We test whether mitochondrial-nuclear incompatibilities have accumulated within the Drosophila melanogaster species subgroup by combining divergent mitochondrial and nuclear lineages and quantifying the effects on relative fitness. Precise placement of nine mtDNAs from D. melanogaster, D. simulans, and D. mauritiana into two D. melanogaster nuclear genetic backgrounds reveals significant mitochondrial-nuclear epistasis affecting fitness in females. Combining the mitochondrial genomes with three different D. melanogaster X chromosomes reveals significant epistasis for male fitness between X-linked and mitochondrial variation. However, we find no evidence that the more than 500 fixed differences between the mitochondrial genomes of D. melanogaster and the D. simulans species complex are incompatible with the D. melanogaster nuclear genome. Rather, the interactions of largest effect occur between mitochondrial and nuclear polymorphisms that segregate within species of the D. melanogaster species subgroup. We propose that a low mitochondrial substitution rate, resulting from a low mutation rate and/or efficient purifying selection, precludes the accumulation of mitochondrial-nuclear incompatibilities among these Drosophila species.


Subject(s)
Cell Nucleus/genetics , DNA, Mitochondrial/genetics , Drosophila melanogaster/genetics , Drosophila/genetics , Epistasis, Genetic , Genes, Insect , Animals , Drosophila/classification , Drosophila/physiology , Drosophila melanogaster/classification , Drosophila melanogaster/physiology , Female , Genetic Fitness , Genetic Linkage , Male , X Chromosome
18.
Trends Ecol Evol ; 25(4): 215-23, 2010 Apr.
Article in English | MEDLINE | ID: mdl-19931208

ABSTRACT

Chromosomal sex determination systems create the opportunity for the evolution of selfish genetic elements that increase the transmission of one sex chromosome at the expense of its homolog. Because such selfish elements on sex chromosomes can reduce fertility and distort the sex ratio of progeny, unlinked suppressors are expected to evolve, bringing different regions of the genome into conflict over the meiotic transmission of the sex chromosomes. Here we argue that recurrent genetic conflict over sex chromosome transmission is an important evolutionary force that has shaped a wide range of seemingly disparate phenomena including the epigenetic regulation of genes expressed in the germline, the distribution of genes in the genome, and the evolution of hybrid sterility between species.


Subject(s)
Biological Evolution , Sex Differentiation/genetics , X Chromosome , Y Chromosome , Animals , Female , Genes , Genomics , Male , Meiosis , Reproduction/genetics , Sex Ratio
19.
Trends Genet ; 23(6): 259-63, 2007 Jun.
Article in English | MEDLINE | ID: mdl-17418445

ABSTRACT

Several recent studies have confirmed that mitochondrial DNA variation and evolution are not consistent with the neutral theory of molecular evolution and might be inappropriate for estimating effective population sizes. Evidence for the action of both positive and negative selection on mitochondrial genes has been put forward, and the complex genetics of mitochondrial DNA adds to the challenge of resolving this debate. The solution could lie in distinguishing genetic drift from 'genetic draft' and in dissecting the physiology of mitochondrial fitness.


Subject(s)
DNA, Mitochondrial/genetics , Genes, Mitochondrial , Selection, Genetic , Evolution, Molecular , Genetic Drift , Genomics , Humans
20.
Evolution ; 59(1): 126-37, 2005 Jan.
Article in English | MEDLINE | ID: mdl-15792233

ABSTRACT

The extent to which natural selection shapes phenotypic variation has long been a matter of debate among those studying organic evolution. We studied the patterns of gene expression polymorphism and divergence in several datasets that ranged from comparisons between two very closely related laboratory strains of mice to comparisons across a considerably longer time scale, such as between humans and chimpanzees, two species of mice, and two species of Drosophila. The results were analyzed and interpreted in view of neutral models of phenotypic evolution. Our analyses used a number of metrics to show that most mRNA levels are evolutionary stable, changing little across the range of taxonomic distances compared. This implies that, overall, widespread stabilizing selection on transcription levels has prevented greater evolutionary changes in mRNA levels. Nevertheless, the range of rates of divergence is large with highly significant differences in the rate and patterns of transcription divergence across functional classes defined on the basis of the gene ontology annotation (primates and mice datasets) or on the basis of the pattern of sex-biased gene expression (Drosophila). Moreover, rates of divergence of sex-biased genes in the contrast between Drosophila species show a distinct pattern from that observed in the contrast between populations of D. melanogaster. Hence, we discuss the time scale of the changes observed and its consequences for the relationship between variation in gene expression within and between species. Finally, we argue that differences in mRNA levels of the magnitudes observed herein could be explained by a remarkably small number of generations of directional selection.


Subject(s)
Drosophila melanogaster/genetics , Evolution, Molecular , Genetic Variation , Mice/genetics , Pan troglodytes/genetics , Animals , Brain , Gene Expression Profiling , Humans , Liver , Oligonucleotide Array Sequence Analysis , Phenotype , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , Selection, Genetic
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