Genetic diversity and fitness in small populations of partially asexual, self-incompatible plants

TL;DR

This study uses genetic modeling and simulations to explore how partial asexuality influences genetic diversity and fitness in small self-incompatible plant populations, revealing decreased allele diversity and increased mutation load.

Contribution

It provides new insights into the population genetics of partially asexual, self-incompatible plants by modeling effects of asexuality on genetic diversity and fitness, considering all relevant factors.

Findings

Partial asexuality decreases S-allele diversity.

Heterozygote excess increases mutation load.

Asexual reproduction can confer fitness advantages in small populations.

Abstract

How self-incompatibility systems are maintained in plant populations is still a debated issue. Theoretical models predict that self-incompatibility systems break down according to the intensity of inbreeding depression and number of S-alleles. Other studies have explored the function of asexual reproduction in the maintenance of self-incompatibility. However, the population genetics of partially asexual, self-incompatible populations are poorly understood and previous studies have failed to consider all possible effects of asexual reproduction or could only speculate on those effects. In this study, we investigated how partial asexuality may affect genetic diversity at the S-locus and fitness in small self-incompatible populations. A genetic model including an S-locus and a viability locus was developed to perform forward simulations of the evolution of populations of various sizes. Drift combined with partial asexuality produced a decrease in the number of alleles at the S-locus. In addition, an excess of heterozygotes was present in the population, causing an increase in mutation load. This heterozygote excess was enhanced by the self-incompatibility system in small populations. In addition, in highly asexual populations, individuals produced asexually had some fitness advantages over individuals produced sexually, because sexual reproduction produces homozygotes of the deleterious allele, contrary to asexual reproduction. Our results suggest that future research on the function of asexuality for the maintenance of self-incompatibility will need to (1) account for whole-genome fitness (mutation load generated by asexuality, self-incompatibility and drift) and (2) acknowledge that the maintenance of self-incompatibility may not be independent of the maintenance of sex itself.