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The Resolution of Sexual Antagonism by Gene …

The resolution of sexual antagonism by gene ..

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which is consistent with the Sexually Antagonistic Gene Hypothesis

Sexually antagonistic selection has been considered in the past –, although its role in evolutionary processes has been generally underestimated; it has however recently received both theoretical and empirical attention due to its potential ubiquity in dioecious species , –. Sexually antagonistic selection is at present recognized as a powerful mechanism through which genetic variation of fitness is maintained despite sexual selection in biological populations, in insects , , , birds , , and mammals , leading to population divergence and possibly speciation , , –. Our findings firmly establish, with a particularly relevant example, the occurrence of sexually antagonistic characters in humans. This point of view may help shift the focus away from male homosexuality per se: rather than concentrating on the sole aspect of the reduced male fecundity that it entails, we can place it within the more general framework of a genetic trait with gender-specific benefit, which may have evolved by increasing the fecundity of females. A consequence of this is that the entire population exhibits a high fecundity variation, and, as we show, the trait can neither disappear nor completely invade the gene pool. Indeed, the GFMH may belong to a possibly wide, but at present still poorly understood, class of sexually antagonistic characters that contribute to the maintenance of the observed genetic variation in human populations. As such characters are mostly expected to have a sex-linked component, the present treatment of the GMFH should provide basic understanding also of the dynamics of any such general sexual antagonistic traits.

Only the model of sexually antagonistic selection involving at least two genes ..

Evolutionary conflicts cause opponents to push increasingly hard and in opposite directions on the regulation of traits. One can see only the intermediate outcome from the balance of the exaggerated and opposed forces. Intermediate expression hides the underlying conflict, potentially misleading one to conclude that trait regulation is designed to achieve efficient and robust expression, rather than arising by the precarious resolution of conflict. Perturbation often reveals the underlying nature of evolutionary conflict. Upon mutation or knockout of one side in the conflict, the other previously hidden and exaggerated push on the trait may cause extreme, pathological expression. In this regard, pathology reveals hidden evolutionary design. We first review several evolutionary conflicts between males and females, including conflicts over mating, fertilization, and the growth rate of offspring. Perturbations of these conflicts lead to infertility, misregulated growth, cancer, behavioral abnormalities, and psychiatric diseases. We then turn to antagonism between the sexes over traits present in both males and females. For many traits, the different sexes favor different phenotypic values, and constraints prevent completely distinct expression in the sexes. In this case of sexual antagonism, we present a theory of conflict between X-linked genes and autosomal genes. We suggest that dysregulation of the exaggerated conflicting forces between the X chromosome and the autosomes may be associated with various pathologies caused by extreme expression along the male–female

The Sexually Antagonistic Genes of Drosophila …

c Millers hypothesis is based on the notion of sexually antagonistic selection ..

Our results, which exclude both overdominance and maternal effects on male offspring, also point to a likely scenario of androphilic phenotypic expression of the GFMH, i.e., an expression that specifically increases the attraction to males in both sexes, rather than inducing a more general phenotipic feminization. Androphilia is indeed consistent in a more natural way with the sexually antagonistic hypothesis, in contrast to the hypothesis of feminizing GFMH or maternal GFMH, which are better associated to the genetic models based respectively on overdominance in males, or on genetic maternal effects, which we considered above. See the remarks on phenotypic expression in for more details. We notice that the conclusion of an androphilic effect of the GFMH in principle allows one to make testable predictions regarding the behavior of GFMH carriers, along the lines for instance of , .

The fact that both the models (4a) and (4b), and only those, fit qualitatively the available empirical data not only establishes the sexually antagonistic character of this human trait, but also indicates the presence of at least one X-linked locus for the GFMH. This agrees with the relation between X-linkage of the GFMH and sexual antagonism also pointed out in . The best qualitative agreement with the data is obtained through model (4b) with two X-linked loci: the subtleties of the observed asymmetries therefore indicate the genetics and inheritance dynamics of the GMFH to be modulated by an X-linked switch activating a further locus on the sexual chromosome, possibly together with other autosomal components not identifiable through our analysis.

gene under sexually antagonistic ..

biased genes are or have been sexually antagonistic.

The previous section reviewed the theory of sexual antagonism for a trait that is expressed in both sexes. In that case, each gene favors a trait that averages the distinct male and female optima. All genes on the autosomes favor an equal weighting of the male and female optima, because the reproductive value of those autosomal genes is the same in both sexes. By contrast, genes on the X chromosome favor weighting the female optimum twice as strongly as the male optimum, because X-linked genes in females have twice the reproductive value of X-linked genes in males.

We expected that if sexually antagonistic selection is a potent force acting upon individual genes, duplication will result in paralog families whose members differ in sex‐biased expression.

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Are People Born Gay? The Biological and Genetic Basis …

Our analysis allows us to draw several conclusions that clarify the basic evolutionary dynamics of the genetic factors influencing human male homosexuality and the related female fecundity increase, resolving a number of open questions. As a main point, we can exclude the GFMH propagation mechanisms based on overdominance (male heterozygote advantage), because none of the models (1b), (5a), (5b) account satisfactorily for the sexual-orientation asymmetries of requirement (B1). At this level of genetic analysis, we can also exclude maternal effects, including maternal genomic imprinting, as they lead too easily to GFMH extinction or fixation, against requirement (A). Only the hypothesis that the GFMH are characterized by sexually antagonistic selection (i.e. the GFMH favor one sex and disfavor the other) produces viable population genetic models (see the case (4) above) leading to the persistence of the trait at low frequencies and capable of accounting for the related pedigree asymmetries. For this reason, predictions of possible widespread diffusion of male homo- or bisexuality in human populations are not warranted, as stable low levels of this character are actually compatible with a broad range of parameters in population genetic models.

Paternal Inheritance of Mitochondrial DNA — NEJM

Then, sexually antagonistic selection is considered through models (4), while overdominance in males, described by assigning an increased fitness to males heterozygous for the allele B residing on the autosome, is considered through models (5). In model (6), which we consider only for independent loci on distinct autosomes, the activator allele A is expressed in males only when inherited from the mother, so as to mimick maternal genomic imprinting effects such as those envisaged in for a multi-locus GFMH. Finally, genetic maternal effects are described through model (7).

How Science Is Helping Us Understand Gender - Magazine

Several proposals have been advanced to explain the origin and permanence of male homosexuality from a genetic standpoint. Kin selection was earlier invoked , , , and later refuted , . Other suggestions followed, the more recent debate being broadly focused on three lines of argument, not all based on genetic factors: overdominance (i.e. male heterozygous advantage, , –), maternal effects on male offspring (such as maternal selection , or maternal genomic imprinting ), and sexually antagonistic selection , , , –. Such proposals open many basic problems regarding the dynamics of the putative GFMH, and call for a satisfactory population genetic treatment of their propagation, which is lacking at present. This issue has been recently addressed , where a number of genetic models inspired by the above hypotheses (overdominance, maternal effects, sexual antagonism) were explored, assuming a single diallelic locus, either autosomal or X-linked, for the GFMH (see also , ).

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