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Geeta Arun, M.

Publications and source records attributed to Geeta Arun, M..

3 recordsLinked to original sources

Estimating the additive genetic variance for relative fitness from changes in allele frequency

The rate of adaptation is equal to the additive genetic variance for relative fitness (VA) in the population. Estimating VA typically involves obtaining suitable measures of fitness on a large number of individuals with known pairwise relatedness. Such data are hard to collect and the results are often sensitive to the definition of fitness used. Here, we present a new method for estimating VA that does not involve making measurements of fitness on individuals, but instead tracks changes in the genetic composition of the population. First, we show that VA can readily be expressed as a function of the genome-wide diversity/linkage disequilibrium matrix and genome-wide expected change in allele frequency due to selection. We then show how independent experimental replicates can be used to infer the expected change in allele frequency due to selection and then estimate VA via a linear mixed model. Finally, using individual-based simulations, we demonstrate that our approach yields precise and accurate estimates over a range of biologically plausible scenarios. Article summaryConventional approaches for estimating the heritable component of fitness variation (VA) have steep methodological, statistical, and even definitional challenges. Here, the authors present a new method that overcomes many of these issue by modelling VA using selection-induced changes to a populations genetic composition. The authors develop novel mathematical theory and an inference approach that uses independent experimental populations derived from the same ancestral population. Individual based simulations show that this method provides unbiased and precise estimates of VA. This opens the door for future studies investigating the genomic distribution of VA, a key factor driving Darwinian evolution.

evolutionary biology↗

Nature and location of modifier alleles determine the resolution of intralocus sexual conflict

When selection favours different levels of expression for a shared trait in males and females, the population is said to be in Intralocus Sexual Conflict (IaSC). In a landmark study, Connallon and Clark (2010) showed that modifiers (alleles at a different locus that alter the expression of the trait under IaSC in a sex-specific manner), effectively resolve IaSC. Their model assumed that modifier alleles are "perfect"; i.e., they fully rescue the harmful effects of the deleterious allele while leaving the positive effects of the beneficial allele unaffected. In the present study, we relaxed this assumption to include more realistic "imperfect" modifier alleles. Imperfect modifiers are those that reduce the expressions of both detrimental allele and beneficial allele to different extents in a given sex. We also ask whether autosomes or X chromosomes are more conducive to resolution of IaSC. Our results suggest that the resolution of IaSC may not always be guaranteed when the modifier allele is "imperfect." Interestingly, IaSC gets resolved more easily on autosomes only when modifier alleles are "perfect" or near "perfect" in concordance with the assumption made by Connallon and Clark (2010). However, in general, X chromosomes are more conducive to the resolution of IaSC.

evolutionary biology↗

Evolutionary genetics of Drosophila melanogaster immunity: role of the X chromosome and sex-specific dominance

Intralocus Sexual Conflict (IaSC) ensues when males and females of the same species experience divergent selection on shared traits. A large number of traits have been implicated in IaSC and there is growing evidence for sexual antagonism associated with immunity. X chromosomes are thought to be hotspots of sexually antagonistic genetic variation and have been shown to harbour substantial immunity-related genetic variation. Here, using interpopulation crosses and cytogenetic cloning, we investigated the role of the X chromosome in improved immune response of laboratory populations of the fruit-fly Drosophila melanogaster selected against systemic infection by Pseudomonas entomophila. We could not detect any contribution of the X chromosome in the evolved immune response of our selected populations. However, we found strong evidence of sex-specific dominance related to immunity in our populations. Our results indicate that alleles that confer a superior immune response to the selected populations are, on average, partially dominant in females but partially recessive in males. We argue that sex-specific dominance over immunity evolved as a by-product of sexually antagonistic selection in the wild ancestors of our populations. We also highlight sex-specific dominance as a potential mechanism of sex differences in immunity, with population-level sex differences primarily driven by sex differences in heterozygotes.

evolutionary biology↗