predeterminación biológica (neurológica o genética) a la homosexualidad, y consiguientemente, de irresponsabilidad o al menos impotencia de revertir la. Síndrome XXY, el trastorno genético que afecta a los genitales y la . lo asocian con la homosexualidad, cuando en realidad no es así”. samente seleccionada, para continuar la combinación genética, la existencia de la homosexualidad y la transexualidad son una para- doja evolutiva. Hay una.
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Homosexuality is a common occurrence in humans and other species, yet its genetic and evolutionary basis is poorly understood. Here, we formulate and study a series of simple mathematical models for the purpose of predicting empirical patterns that can be used to determine the form of selection that homosexalidad to polymorphism of genes influencing homosexuality. Specifically, we develop theory to make contrasting predictions about the genetic characteristics of genes influencing homosexuality including: We conclude that the measurement of the genetic characteristics of quantitative trait loci QTLs found in genomic screens for genes influencing homosexuality can be highly informative in resolving the form of natural selection gemetica their polymorphism.
There are several reasons for the long-standing interest among evolutionary biologists e.
Genetic models of homosexuality: generating testable predictions
Second, there are two lines of evidence that homosexuality is influenced by polymorphic genes: Third, even if one assumes only a small fitness cost to the expression of homosexuality, it appears to be more common in both males and females than can be plausibly explained by mutation—selection balance Kinsey et al.
Maternal effects may contribute to the homosexual phenotype. For example, there is a curious relationship between birth order and the incidence of male homosexuality. There have been a few attempts to localize the specific genes that influence male homosexuality.
The complex nature of the occurrence of male homosexuality in human pedigrees indicates that its inheritance is not a simple Mendelian trait Pillard et al. Recently, a genome-wide QTL screen for male homosexuality Mustanski et al. These initial results are only preliminary and require confirmation from additional genetic studies. Two mechanisms for the maintenance of polymorphism in genes that cause homosexuality have been hommosexualidad frequently mentioned in evolutionary biology literature: Homoseuxalidad potential importance of this mechanism is highlighted by recent data which indicate that female maternal relatives of homosexuals Camperio-Ciani et al.
The topic of homosexuality has so far received only very limited attention in theoretical evolutionary genetics and we are aware of only two previous papers that have attempted to model it.
The second paper was by Getzwho assumed that reduced mating success of homosexual men was compensated by increased rearing success of females or increased joint fecundity and cooperation of couples.
Both these papers studied the case of a single autosomal, diallelic locus, and they concentrated on the conditions for invasion of an allele promoting homosexuality. Our goal is to formulate a series of simple mathematical models for the purpose of predicting empirical patterns that can be used to guide future genetic analysis of homosexuality.
We specifically wanted to generate testable predictions that will provide a foundation for the generation homosfxualidad empirical evidence for or against alternative evolutionary hypotheses for the maintenance of polymorphic genes that influence homosexuality.
Accordingly, we develop theory to make predictions about: Because homosexuality has previously received very little attention in the context of sexually antagonistic alleles, our main focus will be on this model, but we will also extend the previous work homosexualiddad overdominance. Lastly, our approach uses as a foundation extant simple models of sexually antagonistic genes Rice and of maternal and parental selections Gavrilets ; Spencer ; Miller et al.
We will assume throughout that males are the heterogametic sex, but all our results can be applied reciprocally to the case of female heterogamety.
We do not attempt to analyse the altruism towards kin model. Because neither any existing data nor any mathematical models known to us support its plausibility, we consider it premature to include the kin-altruism mechanism in our analysis.
We consider a one-locus, two-allele diploid population with genotypes AAAa and aa. Generations are discrete and non-overlapping. The population size is effectively infinite. Fitness is understood as viability i. Mating is random among the individuals who enter the mating pool. Throughout the manuscript, A is an allele that has little or no influence on sexual orientation, and allele a masculinizes or feminizes both sexes, and thereby increases the probability of homosexuality in the discordant sex.
A feminizing allele a would be one that canalized development towards the female sex-determination pathway. Such an allele would be favoured in females because it protects them when exposed to masculinizing environmental conditions, but this same allele, when expressed in males, would feminize them and could thereby lead to homosexuality. Below, our main focus is on the conditions required for the maintenance of genetic variation.
The dynamic equations describing specific models are given in appendix A. First, we analyse the case when fitness and sexual orientation in both sexes are influenced solely by the direct genetic effects of genes residing in a zygote. In later sections, we will consider the cases, where maternal effects influence these characters.
Assume that the locus under consideration is autosomal. Let female fitnesses be f 1f 2 and f 3 and male fitnesses be m 1m 2 and m 3 in genotypes AAAa and aarespectively.
In this system, the polymorphism is protected i. Note that inequality 3. We consider three different cases. If heterozygotes have the highest fitness in both sexes i. Although overdominance in both sexes is possible, the more plausible scenario for overdominance of a feminizing or masculinizing allele would be overdominance in one sex and directional selection in the other sex, as described subsequently.
However, the same conclusions are reached if the roles of the two sexes are reversed. Here and throughout, primed and unprimed symbols denote fitness effects in opposite sexes. The left-hand side of inequality 3. Overall, overdominance need not be strong to maintain polymorphism. Increasing the degree of dominance h of allele a in females promotes the maintenance of genetic variation; if allele a is dominant in females i.
For illustration, we assume that a feminizing allele a increases the fitness of females but decreases the fitness of males. However, the conclusions are not changed, if the roles of the two sexes are reversed. Then, allele a increases in frequency when rare if. Allele a does not go to fixation if. These conditions are illustrated in figure 1.
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Note that if G is small, the conditions for the maintenance of genetic variation are very strict. Also note that conditions 3. Conditions for the maintenance of genetic variation by sexually antagonistic selection in an autosomal locus. Variation is maintained for parameter values between the two hlmosexualidad.
In the above example, we assumed that the degree of dominance is equal in both sexes. If this is not so, then the most favourable scenario for the maintenance of variation is when allele a is dominant in the sex, where it is advantageous and is recessive in the sex where it is deleterious. Assume that the locus under homosexualidax is X-linked.
Let f 1f 2 and f 3 be fitnesses of females AAAa and aarespectively, and m 1 and m 2 be fitnesses of males A and a. In this model, polymorphism is protected if.
Then, the condition 3. Thus, simple overdominance in females i. Conditions for the maintenance of genetic variation in an X-linked gene when there is overdominance in one sex and directional selection in the other sex. Variation is maintained for parameter values above the solid line see inequality 3. To compare the conditions for the maintenance of genetic variation by overdominance in the cases of autosomal and X-linked genes, let us first rewrite inequality 3. Let us also assume that in the autosomal case, the corresponding gene is recessive i.
These assumptions are conservative in the sense that they narrow the conditions for the maintenance of polymorphism as specified by inequality 3.
Assume that allele a increases female fitness but decreases male fitness. Increasing h genwtica the conditions geneticaa the maintenance of variation see figure 3 a. Homisexualidad for the homosexualidwd of genetic variation by sexually antagonistic selection in an X-linked locus. Variation is maintained for parameter values between the two lines of the same color.
Note that gdnetica second solid thick line coincides with the x -axis. Note that the second solid thin line coincides with the y -axis.
Assume that allele a increases male fitness but decreases female fitness. Decreasing h broadens the conditions for the maintenance of variation see figure 3 a. Next, we consider the case when fitnesses in both sexes are determined by maternal effects i. Let f 1f 2f 3 and m 1m 2m 3 be fitnesses owing to maternal effect influences of daughters and sons of females that are AAAa and aarespectively.
In this model, the polymorphism is protected if conditions 3. Note that because the gene under consideration is expressed in females only, whether it is autosomal or X-linked is irrelevant.
Finally, we consider the case when female fitness is determined exclusively by her genotype while male fitness is determined by a maternal effect. Let f 1f 2 and f 3 be the fitnesses of females AA egnetica, Aa hommosexualidad aa. Let m 1m gendtica and m 3 be the maternally determined fitnesses of their sons.
In homosfxualidad model, the polymorphism is protected. Note that inequality 5. As in the previous case, because the gene under consideration is expressed in females only, whether it is autosomal or X-linked is irrelevant. Then, allele a hhomosexualidad invade if.
In this case, the condition for the invasion of allele a is less strict that that when both fitnesses are determined genetically, but the condition for allele a not getting fixed is more strict. Figure 4 illustrates the conditions for the maintenance of genetic variation in this model.
Note that decreasing h i. Variation is maintained the easiest if allele a is recessive i. Conditions for the maintenance of genetic variation by sexually antagonistic maternal selection. Our population genetic models indicate that genes influencing homosexuality can readily spread and become genegica under a wide range of conditions. One of the main goals in our population genetic analysis of homosexuality was to use theory as a guide to focus future research on the genetic basis of homosexuality.
We were especially interested in determining whether explicit predictions concerning the genetic attributes genomic locations, dominance and effect size of homosexuality genes gejetica distinguish between two of homosexualidaf major competing evolutionary explanations for the maintenance of polymorphic homosexuality genes: Because there is an empirically established maternal effect influencing the expression of homosexuality, we also sought to examine how heritable maternal effects might influence these genetic predictions.