About

Pavitra Muralidhar, PhD, is an Assistant Professor of Ecology and Evolution at The University of Chicago. Her research focuses on various aspects of evolutionary biology, including the polygenic response of sex chromosomes to sexual antagonism, recombination and selection against introgressed DNA, and the mechanisms underlying sex chromosome evolution. She has contributed to understanding how reproductive barriers are reinforced through assortative mating and how dominance shifts influence the likelihood of soft selective sweeps. Her work also explores the dynamics of hybridization during biological invasions and the genetic processes that determine relatedness through recombination. Dr. Muralidhar's research integrates theoretical models and empirical data to advance knowledge in evolutionary genetics and reproductive biology.

Research topics

• Biology
• Genetics
• Evolutionary biology
• Ecology
• Statistics

Selected publications

• Sexually antagonistic environments and the stability of environmental sex determination

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-10

  articleOpen accessSenior authorCorresponding

  Abstract 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.

  PublisherOA PDFDOI

• Chromosome-specific drift under stabilizing selection generates polygenic barriers to sex chromosome turnover

  Proceedings of the National Academy of Sciences · 2026-04-08

  articleOpen access1st authorCorresponding

  While sex chromosome systems show frequent evolutionary transitions in some clades, in many others they show long-term stability. 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 sex-determining 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. The theory generates several testable predictions for the evolution of sex chromosome systems that align well with observed phylogenetic patterns. For example, although chromosome-specific drift acts as a global impediment to sex chromosome turnover, those turnovers that do occur should be more likely to maintain the system of heterogamety than to change it. The theory further predicts a higher rate of transitions from environmental to genetic sex determination, versus the reverse. Finally, the theory shows that the evolution of sexual dimorphism in complex traits can drive long-term sex chromosome stability.

  PublisherDOI

• Quantitative system drift

  Proceedings of the National Academy of Sciences · 2026-03-20 · 1 citations

  articleOpen accessSenior author

  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 mean contributions of individual components are free to drift far from their initial values. Each component's drift, though qualitatively identical to neutral drift, is slower by a factor that depends on the fraction of the system's genetic variance contributed by the component. We further show that symmetric mutation between alleles that increase and decrease components' contributions to the system imposes a weak long-term brake on components' drift. 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 contributions to the trait of different subregions of the genome, such as the chromosomes, can drift despite constraint on the genome-wide value. To indicate the broad applicability of our results, we explore their implications for the evolution of gene expression, selection against interspecific hybrids, selection against turnovers of sex-determining systems, and the division of labor in mutualisms.

  PublisherDOI

• Sex chromosome turnover and mitonuclear conflict drive reproductive isolation

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-04

  preprintOpen accessSenior author

  Identifying the genetic basis of reproductive barriers is essential for understanding the origin and maintenance of biological diversity. While some hybrid incompatibilities evolve as incidental byproducts of divergence, those involving sex chromosomes and mitochondrial-nuclear interactions may arise through predictable pathways shaped by genomic conflict. Yet, the extent to which such interactions drive the evolution of reproductive barriers and speciation in natural populations remains unclear. Here, we use whole-genome resequencing in North American fishes to show that two hybridizing species possess distinct, nonhomologous sex chromosomes. These chromosomes exhibit strong associations with sex, reduced introgression in natural hybrid zones, segregation distortion in backcrosses, and an enrichment of nuclear-encoded mitochondrial genes, indicative of sex-linked mitonuclear incompatibilities. We identify a third, distinct sex chromosome in another hybridizing species, indicating repeated sex chromosome turnover within the clade. Parental crosses and genomic analyses suggest that at least one of these transitions was driven by a recessive female-determining mutation, a rare empirical example of a theoretically predicted but seldom observed mechanism of sex chromosome evolution. Together, these results link genomic architecture to hybrid dysfunction and behavioral isolation, providing strong empirical support for long-standing predictions about the role of sex-linked and cytonuclear incompatibilities in speciation.

  PublisherOA PDFDOI

• Quantitative system drift

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-20 · 3 citations

  preprintOpen accessSenior author

  Abstract 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 component’s drift, though qualitatively similar to neutral drift, is slower by a factor that depends on the fraction of the system’s 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.

  PublisherDOI

• Chromosome-specific drift under stabilizing selection generates polygenic barriers to sex chromosome turnover

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-09-04 · 2 citations

  preprintOpen access1st authorCorresponding

  Abstract 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.

  PublisherOA PDFDOI

• Material removal rate studies on machining of D2 steel in WEDM with brass wire

  AIP conference proceedings · 2023-01-01

  articleSenior author
  PublisherDOI

• Material removal rate studies on machining of D2 steel in WEDM with coated zinc wire

  AIP conference proceedings · 2023-01-01

  article
  PublisherDOI

• Polygenic outcomes of sexually antagonistic selection

  bioRxiv (Cold Spring Harbor Laboratory) · 2023-03-03 · 2 citations

  preprintOpen access1st authorCorresponding

  Abstract 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.

  PublisherOA PDFDOI

• Recombination and selection against introgressed DNA

  Evolution · 2023 · 63 citations

  • Biology
  • Genetics
  • Evolutionary biology

  Introgressed DNA is often deleterious at many loci in the recipient species' genome, and is therefore purged by selection. Here, we use mathematical modeling and whole-genome simulations to study the influence of recombination on this process. We find that aggregate recombination controls the genome-wide rate of purging in the early generations after admixture, when purging is most rapid. Aggregate recombination is influenced by the number of chromosomes and heterogeneity in their size, and by the number of crossovers and their locations along chromosomes. A comparative prediction is that species with fewer chromosomes should purge introgressed ancestry more profoundly, and should therefore exhibit weaker genomic signals of historical introgression. Turning to within-genome patterns, we show that, in species with autosomal recombination in both sexes, more purging is expected on sex chromosomes than autosomes, all else equal. The opposite prediction holds for species without autosomal recombination in the heterogametic sex. Finally, positive correlations between recombination rate and introgressed ancestry have recently been observed within the genomes of several species. We show that these correlations are likely driven not by recombination's effect in unlinking neutral from deleterious introgressed alleles, but by recombination's effect on the rate of purging of deleterious introgressed alleles themselves.

  PublisherDOI

Frequent coauthors

• Carl Veller

  University of Chicago

  20 shared

• Martin A. Nowak

  Harvard University

  7 shared

• George W. A. Constable

  University of York

  5 shared

• David Haig

  Harvard University

  5 shared

• Graham Coop

  University of California, Davis

  5 shared

• Nathaniel B. Edelman

  Yale University

  4 shared

• Prem Prakash Srivastava

  3 shared

• Kelly R. Zamudio

  The University of Texas at Austin

  2 shared

Labs

• Muralidhar labPI