The effect of the reproductive system on mutation load.
J. B. S. Haldane (Amer. Nat. 71, 337-349, 1937) argued that, in equilibrium populations, the effect of deleterious mutation on average fitness depends primarily on the mutation rate and is independent of the severity of the mutations. Specifically, the equilibrium population fitness is e-microH, where microH is the haploid genomic mutation rate. Here we extend Haldane's result to a variety of reproductive systems. Using an analysis based on the frequency of classes of individuals with a specified number of mutations, we show that Haldane's principle holds exactly for haploid sex, haploid apomixis, and facultative haploid sex. In the cases of diploid automixis with terminal fusion, diploid automixis with central fusion, and diploid selfing, Haldane's principle holds exactly for recessive mutations and approximately for mutations with some heterozygous effect. In the cases of K-ploid apomixis, diploid endomitosis, and haplodiploidy, we show that Haldane's principle holds exactly for recessive lethal mutations. In addition we extend Haldane's result to various mixtures of the above-mentioned reproductive systems. In the case of diploid out-crossing sexuals, we do not obtain an exact analytic result, but present arguments and computer simulations which show that Haldane's result extends to this case as well in the limit as the number of loci becomes large. Although diverse reproductive systems are equally fit at equilibrium, different reproductive systems harbor vastly different numbers of recessive genes at equilibrium and we provide estimates of these numbers. These different numbers of mutations may create transient selective pressures on individuals with reproductive systems different from that of the equilibrium population.
Hopf
F A
FA
Optical Sciences Center, University of Arizona, Tucson 85721.
Michod
R E
RE
Sanderson
M J
MJ
D000818:Animals; D005804:Genes, Lethal; D005808:Genes, Recessive; D005828:Genetics, Population; D006801:Humans; D008957:Models, Genetic; D009154:Mutation; D010312:Parthenogenesis; D011157:Population Dynamics; D012641:Selection, Genetic