Dataset Information

Male-benefit sexually antagonistic genotypes show elevated vulnerability to inbreeding.

ABSTRACT: BACKGROUND:There is theoretical and empirical evidence for strong sexual selection in males having positive effects on population viability by serving to purify the genome of its mutation load at a low demographic cost. However, there is also theoretical and empirical evidence for negative effects of sexual selection on female fitness, and therefore population viability, known as the gender load. This can take the form of sexually antagonistic (SA) genetic variation where alleles with a selective advantage in males pose a detriment to female fitness, and vice versa. Here, using seed beetles, we shed light on a previously unexplored manifestation of the gender load: the effect of SA genetic variation on tolerance to inbreeding. RESULTS:We found that genotypes encoding high male, but low female fitness exhibited significantly greater rates of extinction upon enforced inbreeding relative to genotypes encoding high female but low male fitness. Also, genotypes encoding low fitness in both sexes exhibited greater rates of extinction relative to generally high-fitness genotypes (though marginally non-significant), an expected finding attributable to variation in mutation load across genotypes. Despite follow-up investigations aiming to identify the mechanism(s) underlying these findings, it remains unclear whether the gender load and the mutation load have independent consequences for tolerance to inbreeding, or whether these two types of genetic architecture interact epistatically to render male-benefit genetic variation relatively intolerant to inbreeding. CONCLUSIONS:Regardless of the underlying mechanism(s), our results show that male-benefit/female-detriment SA genetic variation poses a previously unseen detriment to population viability due to its elevated vulnerability to inbreeding/homozygosity. This suggests that sexual selection in the context of SA genetic variance for fitness may enhance the gender load on population viability more than previously appreciated, due to selecting for male-benefit SA genetic variation that engenders lineages to extinction upon inbreeding. We note that our results imply that SA alleles that are sexually selected for in males may be underrepresented or even lacking in panels of inbred lines.

SUBMITTER: Grieshop K

PROVIDER: S-EPMC5469140 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Male-benefit sexually antagonistic genotypes show elevated vulnerability to inbreeding.

Grieshop Karl K Berger David D Arnqvist Göran G

BMC evolutionary biology 20170612 1

<h4>Background</h4>There is theoretical and empirical evidence for strong sexual selection in males having positive effects on population viability by serving to purify the genome of its mutation load at a low demographic cost. However, there is also theoretical and empirical evidence for negative effects of sexual selection on female fitness, and therefore population viability, known as the gender load. This can take the form of sexually antagonistic (SA) genetic variation where alleles with a ...[more]

PMID: 28606137

Similar Datasets

Project description:BackgroundMale breast cancer (MBC) represents a poorly characterised group of tumours, the management of which is largely based on practices established for female breast cancer. However, recent studies demonstrate biological and molecular differences likely to impact on tumour behaviour and therefore patient outcome. The aim of this study was to investigate methylation of a panel of commonly methylated breast cancer genes in familial MBCs.Methods60 tumours from 3 BRCA1 and 25 BRCA2 male mutation carriers and 32 males from BRCAX families were assessed for promoter methylation by methylation-sensitive high resolution melting in a panel of 10 genes (RASSF1A, TWIST1, APC, WIF1, MAL, RARβ, CDH1, RUNX3, FOXC1 and GSTP1). An average methylation index (AMI) was calculated for each case comprising the average of the methylation of the 10 genes tested as an indicator of overall tumour promoter region methylation. Promoter hypermethylation and AMI were correlated with BRCA carrier mutation status and clinicopathological parameters including tumour stage, grade, histological subtype and disease specific survival.ResultsTumours arising in BRCA2 mutation carriers showed significantly higher methylation of candidate genes, than those arising in non-BRCA2 familial MBCs (average AMI 23.6 vs 16.6, p = 0.01, 45% of genes hypermethylated vs 34%, p < 0.01). RARβ methylation and AMI-high status were significantly associated with tumour size (p = 0.01 and p = 0.02 respectively), RUNX3 methylation with invasive carcinoma of no special type (94% vs 69%, p = 0.046) and RASSF1A methylation with coexistence of high grade ductal carcinoma in situ (33% vs 6%, p = 0.02). Cluster analysis showed MBCs arising in BRCA2 mutation carriers were characterised by RASSF1A, WIF1, RARβ and GTSP1 methylation (p = 0.02) whereas methylation in BRCAX tumours showed no clear clustering to particular genes. TWIST1 methylation (p = 0.001) and AMI (p = 0.01) were prognostic for disease specific survival.ConclusionsIncreased methylation defines a subset of familial MBC and with AMI may be a useful prognostic marker. Methylation might be predictive of response to novel therapeutics that are currently under investigation in other cancer types.

Project description:Avoiding inbreeding, and therefore avoiding inbreeding depression in offspring fitness, is widely assumed to be adaptive in systems with biparental reproduction. However, inbreeding can also confer an inclusive fitness benefit stemming from increased relatedness between parents and inbred offspring. Whether or not inbreeding or avoiding inbreeding is adaptive therefore depends on a balance between inbreeding depression and increased parent-offspring relatedness. Existing models of biparental inbreeding predict threshold values of inbreeding depression above which males and females should avoid inbreeding, and predict sexual conflict over inbreeding because these thresholds diverge. However, these models implicitly assume that if a focal individual avoids inbreeding, then both it and its rejected relative will subsequently outbreed. We show that relaxing this assumption of reciprocal outbreeding, and the assumption that focal individuals are themselves outbred, can substantially alter the predicted thresholds for inbreeding avoidance for focal males. Specifically, the magnitude of inbreeding depression below which inbreeding increases a focal male's inclusive fitness increases with increasing depression in the offspring of a focal female and her alternative mate, and it decreases with increasing relatedness between a focal male and a focal female's alternative mate, thereby altering the predicted zone of sexual conflict. Furthermore, a focal male's inclusive fitness gain from avoiding inbreeding is reduced by indirect opportunity costs if his rejected relative breeds with another relative of his. By demonstrating that variation in relatedness and inbreeding can affect intra- and inter-sexual conflict over inbreeding, our models lead to novel predictions for family dynamics. Specifically, parent-offspring conflict over inbreeding might depend on the alternative mates of rejected relatives, and male-male competition over inbreeding might lead to mixed inbreeding strategies. Making testable quantitative predictions regarding inbreeding strategies occurring in nature will therefore require new models that explicitly capture variation in relatedness and inbreeding among interacting population members.

Dataset Information

Male-benefit sexually antagonistic genotypes show elevated vulnerability to inbreeding.

Publications

Male-benefit sexually antagonistic genotypes show elevated vulnerability to inbreeding.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets