Biology subjects

Muralidhar, P.

Publications and source records attributed to Muralidhar, P..

10 recordsLinked to original sources

bioRxiv2026

Sexually antagonistic environments and the stability of environmental sex determination

Just as sexually antagonistic genetic variants have different effects on male and female fitness, environmental conditions too can have sexually antagonistic fitness effects. Such Charnov-Bull effects have been invoked to explain the origin and persistence of environmental sex determination (ESD), which allows development of each sex in the environments in which it has a comparative advantage. Here, we study different forms of Charnov-Bull effects to characterize how they shape the evolution and stability of ESD. We show that the precise functional form of Charnov-Bull effects can generate large differences in the vulnerability of ESD systems to the invasion of sex-biasing alleles, as well as in the fate of those alleles if they invade. For some configurations of Charnov-Bull effects, strong sex-biasing alleles are likely to spread to intermediate frequencies, rather than to fixation, resulting in mixed ESD systems in which large genetic effects segregate. Overall, our results indicate that the precise nature of Charnov-Bull effects can play a crucial role in the evolutionary dynamics of ESD.

evolutionary biology↗

bioRxiv2025

Quantitative system drift

We consider a biological system composed of multiple genetically variable components, the combined result of which is a quantitative trait under stabilizing selection for an optimal value. We show mathematically that, while the mean value of the system is ultimately constrained to remain near its optimum, the values of individual components are free to drift far from their initial values. Each components drift, though qualitatively similar to neutral drift, is slower by a factor that depends on the fraction of the systems genetic variance contributed by the component. Our results provide a population-genetic basis for system drift, the concept that individual components of a biological system can evolve despite selective constraint on their combined product. A special case is a single polygenic trait under stabilizing selection, where our results predict that the mean genetic contributions to the trait of different subregions of the genome, such as the chromosomes, can drift despite constraint on the genome-wide genetic value. We explore the implications of this latter result for selection against interspecific hybrids and selection against turnovers of sex-determining systems. We further apply our general results to a continuous public goods game played between two species, where they predict that individual species contributions to a costly public good can drift freely. Finally, we show that symmetric mutation between alleles that increase and decrease components contributions to the system provides a weak long-term brake on components drift.

evolutionary biology↗

bioRxiv2024

Polygenic barriers to sex chromosome turnover

Sex chromosome systems show frequent evolutionary transitions in some clades, but long-term stability in others. Previous explanations of this stasis rely on evolutionary dynamics peculiar to sex chromosomes, such as the accumulation of deleterious mutations on the sex-specific chromosome or sexually antagonistic mutations on either sex chromosome. Here, I show that stabilizing selection on quantitative traits promotes stability of sex chromosome systems. The reason is that stabilizing selection, while keeping the value of the trait near its optimum, allows individual chromosomes contributions to the trait to drift, and this chromosome-specific drift reduces the fitness of the novel sexual genotypes necessarily produced during sex chromosome turnover. Given the ubiquity of stabilizing selection on quantitative traits, chromosome-specific drift could play a pivotal role in preventing the turnover of sex chromosome systems across multiple stages of their evolution and can explain key patterns in the phylogenetic distribution of sex-determining systems.

evolutionary biology↗

bioRxiv2023

Polygenic outcomes of sexually antagonistic selection

Sexual antagonism occurs when males and females have different fitness optima for a phenotype, but are constrained from evolving to these optima because of their shared genome. We study the response of a polygenic phenotype to the onset of sexually antagonistic selection, modeling a phenotype initially under stabilizing selection around an optimum, followed by a sudden divergence of the male and female optima. We observe rapid phenotypic evolution to these new optima via small changes in allele frequencies genome-wide. We study the role of sex chromosomes in this divergence and find that, in the absence of dosage compensation, the X chromosome favors evolution toward the female optimum, inducing co-evolutionary male-biased responses on the autosomes. However, dosage compensation obscures the female-biased interests of the X, causing it to contribute equally to male and female phenotypic change. In both scenarios, we see little effect of dominance in the genetic variation utilized by the X chromosome vs. the autosomes. We go on to examine the dynamics of stabilizing selection once the male and female optima have been reached, exploring a subtle mechanism through which the X chromosome, via the Bulmer effect, can cause higher equilibrium phenotypic variance in males than females. Finally, we consider how sexual antagonistic selection might persist across longer time scales, demonstrating that random fluctuations in an adaptive landscape can generate prolonged intragenomic conflict. Overall, our results provide insight into the response of complex phenotypes to sexually antagonistic selection and the evolution of sexual dimorphism.

evolutionary biology↗

bioRxiv2021

Mate choice enhances post-zygotic barriers to gene flow via ancestry bundling

Hybridization and subsequent genetic introgression are now known to be common features of the histories of many species, including our own. Following hybridization, selection often purges introgressed DNA genome-wide. While mate choice can prevent hybridization in the first place, it is also known to play an important role in post-zygotic selection against hybrids, and thus the purging of introgressed DNA. However, this role is usually thought of as a direct one: a mating preference for conspecifics reduces the sexual fitness of hybrids, reducing the transmission of introgressed ancestry. Here, we explore a second, indirect role of mate choice as a barrier to gene flow. Under assortative mating, parents covary in their ancestry, causing ancestry to be "bundled" in their offspring and later generations. This bundling effect increases ancestry variance in the population, enhancing the efficiency with which post-zygotic selection purges introgressed DNA. Using whole-genome simulations, we show that the bundling effect can comprise a substantial portion of mate choices overall effect as a post-zygotic barrier to gene flow, and that it is driven by ancestry covariances between and within maternally and paternally inherited genomes. We derive a simple method for estimating the impact of the bundling effect from standard measures of assortative mating. Applying this method to data from a diverse set of hybrid zones, we find that the bundling effect increases the purging of introgressed DNA by between 1.2-fold (in a baboon system with weak assortative mating) and 14-fold (in a swordtail system with strong assortative mating). Thus, the bundling effect of mate choice contributes substantially to the genetic isolation of species.

evolutionary biology↗

bioRxiv2021

Dominance shifts increase the likelihood of soft selective sweeps

Genetic models of adaptation to a new environment have typically assumed that the alleles involved maintain a constant fitness dominance across the old and new environments. However, theories of dominance suggest that this should often not be the case. Instead, the alleles involved should frequently shift from recessive deleterious in the old environment to dominant beneficial in the new environment. Here, we study the consequences of these expected dominance shifts for the genetics of adaptation to a new environment. We find that dominance shifts increase the likelihood that adaptation occurs from the standing variation, and that multiple alleles from the standing variation are involved (a soft selective sweep). Furthermore, we find that expected dominance shifts increase the haplotypic diversity of selective sweeps, rendering soft sweeps more detectable in small genomic samples. In cases where an environmental change threatens the viability of the population, we show that expected dominance shifts of newly beneficial alleles increase the likelihood of evolutionary rescue and the number of alleles involved. Finally, we apply our results to a well-studied case of adaptation to a new environment: the evolution of pesticide resistance at the Ace locus in Drosophila melanogaster. We show that, under reasonable demographic assumptions, the expected dominance shift of resistant alleles causes soft sweeps to be the most frequent outcome in this case, with the primary source of these soft sweeps being the standing variation at the onset of pesticide use, rather than recurrent mutation thereafter.

evolutionary biology↗

bioRxiv2020

Variation in genetic relatedness is determined by the aggregate recombination process

The genomic proportion that two relatives share identically by descent--their genetic relatedness-- can vary depending on the history of recombination and segregation in their pedigree. This variation is important in many applications of genetics, including pedigree-based estimation of the genetic variance and heritability of traits, and estimation of pedigree relationships from sequence data. Here, we calculate the variance of genetic relatedness for general pedigree relationships, making no assumptions about the recombination process. For the specific relationships of grandparent-grandoffspring and siblings, the variance of genetic relatedness is a simple decreasing function of [Formula], the average proportion of locus pairs that recombine in meiosis. For general pedigree relationships, the variance of genetic relatedness is likewise the average of some function of pairwise recombination rates. Therefore, features of the aggregate recombination process that affect [Formula] and analogs also affect variance in genetic relatedness. Such features include the number of chromosomes and heterogeneity in their size, and the number of crossovers and their location along chromosomes. Our calculations help to explain several recent observations about variance in genetic relatedness, including that it is reduced by crossover interference (which is known to increase [Formula]). Our methods further allow us to calculate the neutral variance of ancestry among F2s in a hybrid cross, enabling precise statistical inference in F2-based tests for various kinds of selection.

genetics↗

bioRxiv2019

Recombination, variance in genetic relatedness, and selection against introgressed DNA

DNA introgressed from one species into another is typically deleterious at many genomic loci in the recipient species. It is therefore purged by selection over time. Here, we use mathematical modeling and whole-genome simulations to study the influence of recombination on the purging of introgressed DNA. We find that aggregate recombination controls the genome-wide rate of purging in the first few generations after admixture, when purging is most rapid. Aggregate recombination is quantified by [Formula], the average recombination rate across all locus pairs, and analogous metrics. It is influenced by the number of crossovers (i.e., the map length) and their locations along chromosomes, and by the number of chromosomes and heterogeneity in their size. A comparative prediction of our analysis is that species with fewer chromosomes should purge introgressed DNA more profoundly, and therefore should exhibit a weaker genomic signal of historical introgression. With regard to patterns across the genome, we show that, in heterogametic species with autosomal recombination in both sexes, more purging is expected on sex chromosomes than on autosomes, all else equal. The opposite prediction holds for species without autosomal recombination in the heterogametic sex. Finally, we show that positive genomic correlations between local recombination rate and introgressed ancestry, as recently observed in several taxa, are likely driven not by recombinations effect in unlinking neutral from deleterious introgressed alleles, but rather by its effect on the rate of purging of the deleterious alleles themselves. Note on this versionAn earlier version of this manuscript had two parts: (1) Calculations of the variance of genetic relatedness between individuals with particular pedigree relationships, taking into account the randomness of recombination and segregation in their pedigree. (2) An investigation of the rate of purging of introgressed DNA following admixture, based in part on results from part (1). Part (1) has since been published as Veller et al. (2020). The present manuscript has been reconfigured to focus on part (2).

evolutionary biology↗

bioRxiv2019

On the logic of Fisherian sexual selection

In Fishers model of sexual selection, a female preference for a male trait spreads together with the trait because their genetic bases become correlated. This can be interpreted as a greenbeard system: a preference gene, by inducing a female to mate with a trait-bearing male, favors itself because the male is disproportionately likely also to carry the preference gene. Here, we use this logic to argue that Fisherian sexual selection in diploids proceeds via two channels, corresponding to two reasons that trait-bearing males disproportionately carry preference genes: (i) trait-bearing males are disproportionately the product of matings between preference-bearing mothers and trait-bearing fathers, and thus trait and preference genes are correlated in trans; (ii) trait and preference genes come into gametic phase disequilibrium, and thus are correlated in cis. Gametic phase disequilibrium is generated by three distinct mechanisms: a recombination mechanism, a dominance mechanism, and a sexual admixture mechanism. The trans channel does not operate when sexual selection is restricted to the haploid phase, and therefore represents a fundamental difference between haploid and diploid models of sexual selection. We use simulation experiments to artificially eliminate the cis channel, and show that a preference gene can spread in its absence in the diploid model, but not in the haploid model. We further show that the cis and trans channels contribute equally to the spread of the preference when recombination between the preference and trait loci is free, but that the trans channel becomes substantially more important when linkage is tight.

evolutionary biology↗

bioRxiv2017

Drift-Induced Selection Between Male And Female Heterogamety

Evolutionary transitions between male and female heterogamety are common in both vertebrates and invertebrates. Theoretical studies of these transitions have found that, when all genotypes are equally fit, continuous paths of intermediate equilibria link the two sex chromosome systems. This observation has led to a belief that neutral evolution along these paths can drive transitions, and that arbitrarily small fitness differences among sex chromosome genotypes can determine the system to which evolution leads. Here, we study stochastic evolutionary dynamics along these equilibrium paths. We find non-neutrality, both in transitions retaining the ancestral pair of sex chromosomes and in those creating a new pair. In fact, substitution rates are strongly biased in favor of dominant sex determining chromosomes, which fix with higher probabilities than mutations of no effect. Using diffusion approximations, we show that this non-neutrality is a result of drift-induced selection operating at every point along the equilibrium paths: stochastic jumps off the paths return, on average, with a directional bias in favor of the dominant segregating sex chromosome. Our results offer novel explanations for the ubiquity of transitions between male and female heterogamety and the preponderance of dominant major sex determining genes.

evolutionary biology↗