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Sexual Antagonism (sexual + antagonism)
Selected AbstractsSEXUAL ANTAGONISM AND THE EVOLUTION OF X CHROMOSOME INACTIVATIONEVOLUTION, Issue 8 2008Jan Engelstädter In most female mammals, one of the two X chromosomes is inactivated early in embryogenesis. Expression of most genes on this chromosome is shut down, and the inactive state is maintained throughout life in all somatic cells. It is generally believed that X-inactivation evolved as a means of achieving equal gene expression in males and females (dosage compensation). Following degeneration of genes on the Y chromosome, gene expression on X chromosomes in males and females is upregulated. This results in closer to optimal gene expression in males, but deleterious overexpression in females. In response, selection is proposed to favor inactivation of one of the X chromosomes in females, restoring optimal gene expression. Here, we make a first attempt at shedding light on this intricate process from a population genetic perspective, elucidating the sexually antagonistic selective forces involved. We derive conditions for the process to work and analyze evolutionary stability of the system. The implications of our results are discussed in the light of empirical findings and a recently proposed alternative hypothesis for the evolution of X-inactivation. [source] ASSOCIATION BETWEEN SEX RATIO DISTORTION AND SEXUALLY ANTAGONISTIC FITNESS CONSEQUENCES OF FEMALE CHOICEEVOLUTION, Issue 8 2009Tim Connallon Genetic variation can be beneficial to one sex yet harmful when expressed in the other,a condition referred to as sexual antagonism. Because X chromosomes are transmitted from fathers to daughters, and sexually antagonistic fitness variation is predicted to often be X-linked, mates of relatively low-fitness males might produce high-fitness daughters whereas mates of high-fitness males produce low-fitness daughters. Such fitness consequences have been predicted to influence the evolution of female mating biases and the offspring sex ratio. Females might evolve to prefer mates that provide good genes for daughters or might adjust offspring sex ratios in favor of the sex with the highest relative fitness. We test these possibilities in a laboratory-adapted population of Drosophila melanogaster, and find that females preferentially mate with males carrying genes that are deleterious for daughters. Preferred males produce equal numbers of sons and daughters, whereas unpreferred males produce female-biased sex ratios. As a consequence, mean offspring fitness of unpreferred males is higher than offspring fitness of preferred males. This observation has several interesting implications for sexual selection and the maintenance of population genetic variation for fitness. [source] The sexually-selected sperm hypothesis: sexbiased inheritance and sexual antagonismBIOLOGICAL REVIEWS, Issue 2 2002T. PIZZARI ABSTRACT When females are inseminated by more than one male (polyandry) sexual selection continues after insemination in the form of sperm competition and cryptic female choice. The sexually-selected sperm hypothesis proposes that, under the risk of sperm competition, additive variation in male traits determining fertilising effciency will select for female propensity to be polyandrous in order to increase the probability of producing sons with superior fertilising effciency. Two factors complicate this prediction: sex-biased transmission of male fertilising effciency traits and sexual antagonism of sex-limited traits, fostered by sexbiased inheritance. Here, we (i) review the evidence that male traits contributing towards fertilising effciency are heritable through sex-biased mechanisms, and (ii) explore the evolutionary implications for male and female reproductive strategies caused by both sex-biased transmission and sexual antagonism of fertilising effciency traits. Many male fertilising effciency traits are heritable through sex-biased mechanisms and may not necessarily increase female fitness. The predictions of the sexually-selected sperm hypothesis change dramatically under these different mechanisms of inheritance of fertilising effciency traits, and different fitness pay-offs derived by females from the expression of such traits. Both sex-biased control of fertilising effciency and sexual antagonism may also be important in explaining the maintenance of the genetic variance and selection potential of fertilising effciency. We propose that a useful approach to test the sexually-selected sperm hypothesis is to combine studies which identify behavioural and physiological mechanisms explaining variation in reproductive success with artificial selection experiments to infer the underlying evolutionary patterns. [source] | ||||||||||