Limits to Adaptation in Partially Selfing Species
2016 (English)In: Genetics, ISSN 0016-6731, E-ISSN 1943-2631, Vol. 203, no 2, 959-+ p.Article in journal (Refereed) PublishedText
In outcrossing populations, "Haldane's sieve" states that recessive beneficial alleles are less likely to fix than dominant ones, because they are less exposed to selection when rare. In contrast, selfing organisms are not subject to Haldane's sieve and are more likely to fix recessive types than outcrossers, as selfing rapidly creates homozygotes, increasing overall selection acting on mutations. However, longer homozygous tracts in selfers also reduce the ability of recombination to create new genotypes. It is unclear how these two effects influence overall adaptation rates in partially selfing organisms. Here, we calculate the fixation probability of beneficial alleles if there is an existing selective sweep in the population. We consider both the potential loss of the second beneficial mutation if it has a weaker advantage than the first one, and the possible replacement of the initial allele if the second mutant is fitter. Overall, loss of weaker adaptive alleles during a first selective sweep has a larger impact on preventing fixation of both mutations in highly selfing organisms. Furthermore, the presence of linked mutations has two opposing effects on Haldane's sieve. First, recessive mutants are disproportionally likely to be lost in outcrossers, so it is likelier that dominant mutations will fix. Second, with elevated rates of adaptive mutation, selective interference annuls the advantage in selfing organisms of not suffering from Haldane's sieve; outcrossing organisms are more able to fix weak beneficial mutations of any dominance value. Overall, weakened recombination effects can greatly limit adaptation in selfing organisms.
Place, publisher, year, edition, pages
2016. Vol. 203, no 2, 959-+ p.
adaptation, selection interference, dominance, self-fertilization, recombination
IdentifiersURN: urn:nbn:se:uu:diva-299057DOI: 10.1534/genetics.116.188821ISI: 000377462800028PubMedID: 27098913OAI: oai:DiVA.org:uu-299057DiVA: diva2:948784