Altruism, sex, and inbreeding when the genotype–phenotype map is additive

Recently published theoretical results suggest that, in a sexual population, when genotypes code for phenotypes in a complex manner, it is possible for altruistic genotypes to spread through a metapopulation (i.e. through a collection of subpopulations). This spread tends to occur during periods when the environment deteriorates throughout the metapopulation. By contrast, under asexual reproduction, non-altruistic genotypes seem to be favoured, at least when subpopulations are substantial in size. The most relevant previous study makes use of Kauffman and Levin's “NK model” as a way to relate genotypes to fitness. Unfortunately, there are both conceptual and technical problems with the application of the NK model to populations that contain many different genotypes (e.g. polymorphic diploid populations with more than a few loci under selection). The present study presents a more tractable and biologically plausible model to study the causal relationship between sexual reproduction and altruism. In particular, phenotypes are determined by additive interactions among alleles at different loci in a diploid genome, with up to 200 loci under selection. In addition, subpopulations are substantially larger than those considered in the most relevant previous work. The results show that, so long as there are multiple “fitness peaks” in “phenotype space”, the additive genotype–phenotype map leads to results that are similar to those from the NK model. Various parameters are manipulated in an effort to discover the determinants of altruistic and non-altruistic outcomes. The findings should facilitate further investigations, and they should help to establish the plausibility of the suggested relationship between sexual reproduction and altruism. The results also suggest that inbreeding can lead to a similar result as asexuality. That is, inbreeding seems to enhance the probability that altruistic phenotypes will be eliminated.