Signatures of sexually antagonistic selection in sex-specific dominance of gene expression
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ABSTRACT:
PROVIDER: PRJEB70958 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12383300_1.fastq.gz | Fastqsanger.gz | |||
| ERR12383300_2.fastq.gz | Fastqsanger.gz | |||
| ERR12383301_1.fastq.gz | Fastqsanger.gz | |||
| ERR12383301_2.fastq.gz | Fastqsanger.gz | |||
| ERR12383302_1.fastq.gz | Fastqsanger.gz |
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Project description:Differences in the selective pressures experienced by males and females are believed to be ubiquitous in dioecious organisms and are expected to result in the evolution of sexually antagonistic alleles, thereby driving the evolution of sexual dimorphism. Negative genetic correlation for fitness between the sexes has been documented, however, the identity, number and location of loci causing this relationship are unknown. Here we show that a large proportion of Drosophila melanogaster transcripts are associated with the interaction between genomic haplotype and gender and that at least 8% of loci in the fly genome are currently evolving under sexually antagonistic selection.
2010-02-10 | GSE17013 | GEO
Project description:Differences in the selective pressures experienced by males and females are believed to be ubiquitous in dioecious organisms and are expected to result in the evolution of sexually antagonistic alleles, thereby driving the evolution of sexual dimorphism. Negative genetic correlation for fitness between the sexes has been documented, however, the identity, number and location of loci causing this relationship are unknown. Here we show that a large proportion of Drosophila melanogaster transcripts are associated with the interaction between genomic haplotype and gender and that at least 8% of loci in the fly genome are currently evolving under sexually antagonistic selection. We measured gene expression of adult males and females of Drosophila melanogaster from 15 hemiclone lines, showing either high-male/low-female fitness, high-female/lowmale fitness or average fitness in both sexes. Data from four replicates for each sex/line are presented, giving a total of 120 arrays.
2010-02-10 | E-GEOD-17013 | biostudies-arrayexpress
Project description:Several lines of evidence indicate the existence of genetic factors influencing male homosexuality and bisexuality. In spite of its relatively low frequency, the stable permanence in all human populations of this apparently detrimental trait constitutes a puzzling 'Darwinian paradox'. Furthermore, several studies have pointed out relevant asymmetries in the distribution of both male homosexuality and of female fecundity in the parental lines of homosexual vs. heterosexual males. A number of hypotheses have attempted to give an evolutionary explanation for the long-standing persistence of this trait, and for its asymmetric distribution in family lines; however a satisfactory understanding of the population genetics of male homosexuality is lacking at present. We perform a systematic mathematical analysis of the propagation and equilibrium of the putative genetic factors for male homosexuality in the population, based on the selection equation for one or two diallelic loci and Bayesian statistics for pedigree investigation. We show that only the two-locus genetic model with at least one locus on the X chromosome, and in which gene expression is sexually antagonistic (increasing female fitness but decreasing male fitness), accounts for all known empirical data. Our results help clarify the basic evolutionary dynamics of male homosexuality, establishing this as a clearly ascertained sexually antagonistic human trait.
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Project description:Since the autosomal genome is shared between the sexes, sex-specific fitness optima present an evolutionary challenge. While sexually antagonistic selection might favor different alleles within females and males, segregation randomly reassorts alleles at autosomal loci between sexes each generation. This process of homogenization during transmission thus prevents between-sex allelic divergence generated by sexually antagonistic selection from accumulating across multiple generations. However, recent empirical studies have reported high male-female FST statistics. Here, we use a population genetic model to evaluate whether these observations could plausibly be produced by sexually antagonistic selection. To do this, we use both a single-locus model with nonrandom mate choice, and individual-based simulations to study the relationship between strength of selection, degree of between-sex divergence, and the associated genetic load. We show that selection must be exceptionally strong to create measurable divergence between the sexes and that the decrease in population fitness due to this process is correspondingly high. Individual-based simulations with selection genome-wide recapitulate these patterns and indicate that small sample sizes and sampling variance can easily generate substantial male-female divergence. We therefore conclude that caution should be taken when interpreting autosomal allelic differentiation between the sexes.
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Project description:Sex estimation of human remains from demineralized blocks of tooth enamel by liquid chromatography tandem mass spectrometry (LC- MS/MS) and proteomic analysis of sexually dimorphic amelogenin peptides. The detection of the Y-isoform of amelogenin is used to estimate male sex. The combined signal intensity of the sexually dimorphic peptides from each samples of known sex is used to establish a statistical framework for the estimation of the female sex probability.
2018-11-29 | PXD009781 | Pride
Project description:Genomic conflict is perplexing because it causes the fitness of a species to decline rather than improve. Many diverse forms of genomic conflict have been identified, but this extant tally may be incomplete. Here, we show that the unusual characteristics of the sex chromosomes can, in principle, lead to a previously unappreciated form of sexual genomic conflict. The phenomenon occurs because there is selection in the heterogametic sex for sex-linked mutations that harm the sex of offspring that does not carry them, whenever there is competition among siblings. This harmful phenotype can be expressed as an antagonistic green-beard effect that is mediated by epigenetic parental effects, parental investment, and/or interactions among siblings. We call this form of genomic conflict sexually antagonistic "zygotic drive", because it is functionally equivalent to meiotic drive, except that it operates during the zygotic and postzygotic stages of the life cycle rather than the meiotic and gametic stages. A combination of mathematical modeling and a survey of empirical studies is used to show that sexually antagonistic zygotic drive is feasible, likely to be widespread in nature, and that it can promote a genetic "arms race" between the homo- and heteromorphic sex chromosomes. This new category of genomic conflict has the potential to strongly influence other fundamental evolutionary processes, such as speciation and the degeneration of the Y and W sex chromosomes. It also fosters a new genetic hypothesis for the evolution of enigmatic fitness-reducing traits like the high frequency of spontaneous abortion, sterility, and homosexuality observed in humans.
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Project description:Due to its hemizygous mode of inheritance and role in sex determination, the X chromosome is expected to play an important role in the evolution of sexual dimorphism, and to be enriched for sexually antagonistic genetic variation. By forcing the X chromosome to only be expressed in males over many generations, we changed the selection pressures on the X to become similar to those experienced by the Y chromosome. This releases the X from any constraints arising from selection in females, and is predicted to lead to specialization for male fitness, including masculinization of phenotypes that normally experience sexually antagonistic selection. Indeed, we found evidence of this via upregulation of male-benefit sexually antagonistic genes, and downregulation of X-linked female benefit genes. Interestingly, we could detect evidence of microevolutionary changes consistent with previously documented patterns of macroevolutionary change, such as changes in expression consistent with previously established patterns of sexual dimorphism, an increase in the expression of metabolic genes related to mitonuclear conflict, and evidence that dosage compensation constitutes a constraint for male-benefit genes. These results confirm the importance of the X in the evolution of sexual dimorphism and as a source for sexually antagonistic genetic variation, and demonstrate that experimental evolution can be a fruitful method for testing theories of sex chromosome evolution. Microarray data was used to detect differences in gene expression as result of experimental evolution.
2018-12-14 | GSE123827 | GEO
Project description:Genetic variance (VG) in fitness related traits is often unexpectedly high, evoking the question how VG can be maintained in the face of selection. Sexually antagonistic (SA) selection favouring alternative alleles in the sexes is common and predicted to maintain VG, while directional selection should erode it. Both SA and sex-limited directional selection can lead to sex-specific adaptations but how each affect VG when sexual dimorphism evolves remain experimentally untested. Using replicated artificial selection on the seed beetle Callosobruchus maculatus body size we recently demonstrated an increase in size dimorphism under SA and male-limited (ML) selection by 50% and 32%, respectively. Here we test their consequences on genetic variation. We show that SA selection maintained significantly more ancestral, autosomal additive genetic variance than ML selection, while both eroded sex-linked additive variation equally. Ancestral female-specific dominance variance was completely lost under ML, while SA selection consistently sustained it. Further, both forms of selection preserved a high genetic correlation between the sexes (rm,f). These results demonstrate the potential for sexual antagonism to maintain more genetic variance while fuelling sex-specific adaptation in a short evolutionary time scale, and are in line with predicted importance of sex-specific dominance reducing sexual conflict over alternative alleles.
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Project description:Antagonistic interactions between the sexes are important drivers of evolutionary divergence. Interlocus sexual conflict is generally described as a conflict between alleles at two interacting loci whose identity and genomic location are arbitrary, but with opposite fitness effects in each sex. We build on previous theory by suggesting that when loci under interlocus sexual conflict are located on the sex chromosomes it can lead to cycles of antagonistic coevolution between them and therefore between the sexes. We tested this hypothesis by performing experimental crosses using Drosophila melanogaster where we reciprocally exchanged the sex chromosomes between five allopatric wild-type populations in a round-robin design. Disrupting putatively coevolved sex chromosome pairs resulted in increased male reproductive success in 16 of 20 experimental populations (10 of which were individually significant), but also resulted in lower offspring egg-to-adult viability that affected both male and female fitness. After 25 generations of experimental evolution these sexually antagonistic fitness effects appeared to be resolved. To formalize our hypothesis, we developed population genetic models of antagonistic coevolution using fitness expressions based on our empirical results. Our model predictions support the conclusion that antagonistic coevolution between the sex chromosomes is plausible under the fitness effects observed in our experiments. Together, our results lend both empirical and theoretical support to the idea that cycles of antagonistic coevolution can occur between sex chromosomes and illustrate how this process, in combination with autosomal coadaptation, may drive genetic and phenotypic divergence between populations.
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Project description:The ubiquity of recombination in nature is a paradox because it breaks up combinations of alleles favored by natural selection. Theoretical work has shown that antagonistic coevolution between hosts and parasites can result in rapid fluctuations in epistasis that can create a short-term advantage to recombination. Here, we show that another kind of antagonistic coevolution, interlocus sexually antagonistic coevolution (SAC), can also create indirect selection for modifiers that increase the rate of recombination, and that it can lead to very high levels of recombination at equilibrium. Recombination is favored because interlocus SAC creates heterogeneity in the strength and direction of selection, both within and between generations, which maintains an excess of disadvantageous haplotypes in the population. This result is similar to and consistent with dynamics of fluctuating epistasis produced in models of host-parasite coevolution. However, the conditions under which interlocus SAC provides an advantage to recombination are more permissive.
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