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Evolution. 2014 Dec;68(12):3555-69. doi: 10.1111/evo.12536. Epub 2014 Nov 20.

Sexually antagonistic polymorphism in simultaneous hermaphrodites.

Author information

1
Ashworth Laboratories, Institute of Evolutionary Biology, The University of Edinburgh, Kings Buildings, West Mains Road, Edinburgh, EH9 3JT, United Kingdom. crispin.jordan@ed.ac.uk.

Abstract

In hermaphrodites, pleiotropic genetic trade-offs between female and male reproductive functions can lead to sexually antagonistic (SA) selection, where individual alleles have conflicting fitness effects on each sex function. Although an extensive theory of SA selection exists for dioecious species, these results have not been generalized to hermaphrodites. We develop population genetic models of SA selection in simultaneous hermaphrodites, and evaluate effects of dominance, selection on each sex function, self-fertilization, and population size on the maintenance of polymorphism. Under obligate outcrossing, hermaphrodite model predictions converge exactly with those of dioecious populations. Self-fertilization in hermaphrodites generates three points of divergence with dioecious theory. First, opportunities for stable polymorphism decline sharply and become less sensitive to dominance with increased selfing. Second, selfing introduces an asymmetry in the relative importance of selection through male versus female reproductive functions, expands the parameter space favorable for the evolutionary invasion of female-beneficial alleles, and restricts invasion criteria for male-beneficial alleles. Finally, contrary to models of unconditionally beneficial alleles, selfing decreases genetic hitchhiking effects of invading SA alleles, and should therefore decrease these population genetic signals of SA polymorphisms. We discuss implications of SA selection in hermaphrodites, including its potential role in the evolution of "selfing syndromes."

KEYWORDS:

Adaptation; balancing selection; fitness trade-off; genetic hitchhiking; intralocus sexual conflict; sexual dimorphism

PMID:
25311368
PMCID:
PMC4448763
DOI:
10.1111/evo.12536
[Indexed for MEDLINE]
Free PMC Article

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