Adaptation and Self–Fertilisation
Many organisms are hermaphrodites that are capable of self-fertilisation, where individuals produce both male and female sex cells that can fertilise one another. This mating mode lies in contrast to outcrossing, where individuals reproduce with a different partner. The degree of self-fertilisation affects the promotion of adaptive mutations; for example, recessive mutations (those that only have an appreciable fitness advantage when present as two copies within individuals) are more likely to spread in selfing organisms than in outcrossing ones. Yet the effects that linked mutations have on the spread of adaptive mutations, and the genetic footprint they leave in genome sequence data obtained from self-fertilisation organisms, remain understudied topics. I will first discuss mathematical models to quantify how the spread of beneficial mutations affect selection acting on other linked selected mutations. Higher self-fertilisation rates increase the probability that linked deleterious mutations will spread alongside beneficial mutations. When considering a distribution of deleterious mutations, beneficial mutations generally need to be more recessive than predicted from single-locus results, for selfers to have higher overall fitness than outcrossers following a selective sweep. If recurrent adaptive mutation arises at a target site, then intermediate selfing rates maximize the probability that linked recessive beneficial mutations will spread in a population. I will end by presenting results on the genetic footprint of adaptive mutations for different levels of dominance and self-fertilisation.