Abstract
AbstractMale mice who are heterozygous for distorting and non-distorting alleles at thet-haplotype transmit the drivingt-haplotype around 90% of the time – a drastic departure from Mendelian expectations. This selfish act comes at a cost. The mechanism underlying transmission distortion in this system causes severe sterility in males homozygous for the drive alleles, ultimately preventing its fixation. Curiously, many drivingt-haplotypes also induce embryonic lethality in both sexes when homozygous, however, this is neither universal nor a necessity for this distortion mechanism. Charlesworth provided an adaptive explanation for the evolution of lethalt-haplotypes in a population segregating for distorting and non-distortingtalleles – namely, if mothers compensate by replacing dead embryos with new offspring (or by transferring energy to surviving offspring), a recessive lethal can be favored because it effectively allows mothers the opportunity to trade in infertile males for potentially fertile offspring. However, this model requires near complete reproductive compensation for the invasion of the lethalt-haplotype and produces an equilibrium frequency of lethal drivers well below what is observed in nature. We show that even low levels of systemic inbreeding, which we model as brother-sister mating, allows lethalt-haplotypes to invade with much lower levels of reproductive compensation. Furthermore, inbreeding allows these lethal haplotypes to largely displace the ancestral male-sterile haplotypes. Our results show that together inbreeding and reproductive compensation move expected equilibria closer to observed haplotype frequencies in natural populations and occur under more reasonable parameter combinations.
Publisher
Cold Spring Harbor Laboratory