Biology subjects

Brud, E.

Publications and source records attributed to Brud, E..

8 recordsLinked to original sources

bioRxiv2026

The geometry of dominance shows broad potential for stable polymorphism under antagonistic pleiotropy

Alleles with opposing effects on fitness characters are said to exhibit selectional antagonistic pleiotropy (broadly construed so that effects are not necessarily confined to the same individual). A number of theoretical investigations considered the case where a pair of alleles at a locus influences two fitness components and derived the conditions giving rise to stable polymorphism under various assumptions about the mode of trait-interaction. Strikingly, many of these analyses concluded that the potential for maintaining polymorphism is strongly constrained by the joint influence of two factors: (1) the prevalence of weak selection coefficients over coefficients of large magnitude, and (2) the absence of beneficial dominance reversals (where the deleterious effects of each allele are partially or completely masked in the heterozygous genotype). Consequently, the conclusion that selective polymorphism is unlikely to be maintained by intralocus mechanisms of antagonistic pleiotropy has achieved widespread acceptance. Here we argue that such conclusions do not apply to any of the following models of antagonism: (i) additive trait-interaction, (ii) multiplicative trait-interaction, (iii) bivoltine selection, (iv) soft selection, (v) hard selection, and (vi) sexual antagonism. We demonstrate that the parameter space giving rise to stable allelic variation is quite large throughout, and moreover, the plenitude of suitable parameters neither depends on the strength of selection nor requires dominance reversal. Dominance coefficients associated with stringent conditions for stable polymorphism are shown to be atypical as compared to all feasible parameters, and best regarded as an outcome of adherence to a special relation: dominance with a constant magnitude and direction, which includes the case of additive allelic effects at a locus. Properties of single-locus equilibria (heterozygosity, allele frequency differentiation) are investigated, as well as the contribution of dominance schemes to the genetic variance in fitness characters in populations at multilocus linkage equilibrium. Author summaryAllelic variants at a locus with opposing effects on multiple fitness components (antagonistic fitness pleiotropy) have long been appreciated as a possible source of balancing selection. The prevalence of polymorphism owing to this form of natural selection, however, has been doubted on theoretical grounds due to the fact that standard assumptions of genetic models (namely, constant magnitudes for the dominance coefficients) are hardly conducive to the maintenance of polymorphism. The major exception to this conclusion lies with schemes that exhibit dominance reversal (where the direction of dominance for antagonistic alleles flips across fitness components). Here we conduct a geometric analysis of the space of polymorphism-promoting dominance parameters and conclude that the conditions for maintaining balanced alleles is unrestrictive, with non-reversals playing an underappreciated role.

evolutionary biology↗

bioRxiv2025

Gene flow weakens genomic clines while selection maintains adaptive loci: two decades of evolution in Drosophila melanogaster natural populations

Spatial genetic clines suggest local adaptation, but whether they persist or erode over evolutionary time remains largely unknown. Here, we use a unique genomic time series collected over several decades to quantify how gene flow and selection jointly shape spatial genomic structure. We analyzed pooled whole-genome sequencing from 16 natural populations of Drosophila melanogaster sampled along the North American east coast between 1997 and 2023, spanning hundreds of generations. We find pronounced homogenization of populations over time, accompanied by a genome-wide loss of clinal variants. Polymorphisms that remained clinal were less steep on chromosome 3R, reflecting declines in the frequency and clinality of major chromosomal inversions. Genomic context modulates this process: clinal SNPs are preferentially lost in regions of high recombination, whereas remaining clines are increasingly concentrated in coding and splice-associated sites. Despite widespread erosion of spatial structure, we detect signatures of selection shared across space at detoxification loci, including cytochrome P450 genes linked to insecticide resistance. Together, our results show widespread homogenization of neutral spatial variation consistent with gene flow, while spatially varying selection has preserved a subset of functionally important loci.

evolutionary biology↗

bioRxiv2025

A network perspective on the evolution of hybrid incompatibilities

Theory predicts that hybrid incompatibilities accumulate faster than linearly with genetic divergence, a phenomenon known as the snowball effect. While this prediction is mathematically robust under simplifying assumptions, accumulating evidence suggests that the structure of gene interaction networks can alter both the rate and organization of incompatibility evolution. Here, we extend classic DMI models with a network approach, equating the assumptions of the Orr model with a complete graph of gene interactions. We simulate the evolution of hybrid incompatibilities under different gene interaction networks and evaluate the effects of network density, topology, and substitution model. We find that network density strongly governs the rate of DMI accumulation, particularly under models permitting multiple substitutions per locus, while network topology shapes the agglomeration of incompatibilities into large, connected clusters. Substitution rate heterogeneity, especially when anti-correlated with node degree, further suppresses both accumulation and clustering. These results highlight that while the snowball effect remains qualitatively valid, the structure and evolution of the incompatibility network exhibit nontrivial departures from previous expectations, with implications for observable quantities in empirical systems. Our findings underscore the importance of incorporating genomic architecture and network constraints into models of speciation.

evolutionary biology↗

bioRxiv2023

Dominance and the potential for seasonally balanced polymorphism

Seasonality causes intraannual fitness changes in multivoltine populations (defined as having multiple generations per year). While it is well-known that seasonally balanced polymorphism is established by overdominance in geometric mean fitness, an unsettled aspect of the deterministic theory is the relative contribution of various season-specific dominance mechanisms to the potential for polymorphism. In particular, the relative importance of seasonally-reversing and non-reversing schemes remains unclear. Here I analyze the parameter space for the discrete generation two-season multivoltine model and conclude that, in general, a substantial fraction of stabilizing schemes are non-reversing with the season ([~]25-50%). In addition, I derive the approximate equilibrium allele frequency cycle under bivoltinism, and find that the amplitude of allelic oscillation is maximized by non-reversing dominance if the selection coefficients are roughly symmetric. Lastly, I derive conditions for the intralocus evolution of dominance. These predict a long-term trend toward maximally beneficial reversal. Overall, the results counter the disproportionate emphasis placed on dominance reversal as a stabilizing mechanism and clarify that non-reversing dominance is expected to frequently characterize seasonally fluctuating alleles under both weak and strong selection, especially in their early history. I conclude that seasonally alternating selection regimes are easily able to maintain allelic variation without restrictive assumptions on either selection coefficients or dominance parameters.

evolutionary biology↗

bioRxiv2022

Sign-epistatic centromere drive in panmictic populations

Comparative work has revealed a highly non-random elevation of karyotypic homogeneity within mammalian species for either telocentric chromosomes or centric fusions, and a karyotypic bimodality among species for these binary chromosome morphologies. A verbal theory developed by Pardo-Manuel de Villena and Sapienza argues that morphology-biased segregation in female meiosis explains the corresponding directional evolution in favor of one or the other chromosome form within species, and moreover, periodic reversals of meiotic spindle asymmetry explain the pattern of bimodality observed among species. Here I investigate a population genetic model in which I assume that the direction of the spindle asymmetry is under the control of a modifier gene, either linked or unlinked to a focal karyotypic mutant (linkage being to a centric fusion, say), and I derive the corresponding invasion conditions for the modifier-centric-fusion gene complex. I demonstrate that the scenario put forth in the verbal theory can be explained by a two-step process in which (1) a centric-fusion invades to fixation while the linked modifier winds up at an intermediate frequency by hitchhiking, and then (2) subsequent fixations of unlinked centric fusions occur. Via numerical iteration of the model, I demonstrate that the typical post-hitchhiking frequency of the linked modifier (from step 1) is broadly sufficient for subsequent unlinked invasions (step 2). Sign-reversing modifier evolution is therefore concluded to be a plausible mechanism instantiating the principles of a female drive theory of karyotype evolution.

evolutionary biology↗

bioRxiv2020

Florida Drosophila melanogaster genomes sampled 13 years apart show increases in warm-associated SNP alleles

We studied genetic change in Drosophila melanogaster using whole-genome SNP data from samples taken 13 years apart in Homestead, FL. This population is at the southern tip of a well-studied US latitudinal cline. On the non-inversion-carrying chromosome arms, 11-16% of SNPs show significant frequency changes. These are enriched for latitudinal clines and genic sites. For clinal SNPs each allele is either the northern- or southern-favored. Seventy-eight to 95 percent with significant frequency increase are southern-favored. Five to seven percent of SNPs also show significant seasonal change and involve increases in the northern-favored allele during the season. On the 2L and 3R chromosome arms there are significant seasonal shifts for common inversions. We identify regions and genes that are candidates for selection. These regions also show correspondence with those associated with soft sweeps in Raleigh, NC. This shift towards southern-favored alleles may be caused by climate shifts or increased African-European admixture.

evolutionary biology↗

bioRxiv2019

Adaptive meiotic drive in selfing populations with heterozygote advantage

The egalitarian allotment of gametes to each allele at a locus (Mendels law of segregation) is a near-universal phenomenon characterizing inheritance in sexual populations. As exceptions to Mendels law are known to occur, one can investigate why non-Mendelian segregation is not more common using modifier theory. Earlier work assuming sex-independent modifier effects in a random mating population with heterozygote advantage concluded that equal segregation is stable over long-term evolution. Subsequent investigation, however, demonstrated that the stability of the Mendelian scheme disappears when sex-specific modifier effects are allowed. Here I derive invasion conditions favoring the repeal of Mendelian law in mixed and obligate selfing populations. Oppositely-directed segregation distortion in the production of male and female gametes is selected for in the presence of overdominant fitness. The conditions are less restrictive than under panmixia in that strong selection can occur even without differential viability of reciprocal heterozygotes (i.e. in the absence of parent-of-origin effects at the overdominant fitness locus). Generalized equilibria are derived for full selfing.

evolutionary biology↗

bioRxiv2018

Support for the dominance theory in Drosophila transcriptomes

Interactions among divergent elements of transcriptional networks from different species can lead to misexpression in hybrids through regulatory incompatibilities, some with the potential to generate sterility. Genes with male-biased expression tend to be overrepresented among genes misexpressed in hybrid males. While the possible contribution of faster-male evolution to this misexpression has been explored, the role of the hemizygous X chromosome (i.e., the dominance theory for transcriptomes) remains yet to be determined. Here we study genome-wide patterns of gene expression in females and males of Drosophila yakuba and D. santomea and their hybrids. We used attached-X stocks to specifically test the dominance theory, and we uncovered a significant contribution of recessive alleles on the X chromosome to hybrid misexpression. Our analysis of gene expression patterns suggests that there is a contribution of weakly deleterious regulatory mutations to gene expression divergence in the sex towards which the expression is biased. In the opposite sex (e.g., genes with female-biased expression analyzed in male transcriptomes), we detect stronger selective constraints on gene expression divergence. Although genes with high degree of male-biased expression show a clear signal of faster-X evolution for gene expression divergence, we also detected slower-X evolution of gene expression in other gene classes (e.g. female-biased genes) that is mediated by significant decreases of cis- and trans-regulatory divergence. The distinct behavior of X-linked genes with high degree of male-biased expression is consistent with these genes experiencing a higher incidence of positively selected regulatory mutations than their autosomal counterparts. We propose that both dominance theory and faster-X evolution of gene expression may be major contributors to hybrid misexpression and possibly the large X-effect in these species.

evolutionary biology↗