Meeting Abstract
Although mitochondria are predominantly inherited maternally, empirical results suggest that hybridization often elicits paternal mitochondrial transmission. Thus, it is possible that hybridization, through separation of co-evolved mito-nuclear epistatic loci, causes dysfunction of processes involved in paternal mitochondrial elimination. Evidence from the nematode Caenorhabditis briggsae, a relative of C. elegans, suggests that paternal mitochondrial transmission occurs during the production of intra-species cytoplasmic-nuclear hybrids (cybrids). These hybrids, in which the mitochondrial genome of one population is combined with the nuclear genome of another, sustain paternal “leakage” at fertilization, and thereafter cybrids often fix the paternal mitotype. This pattern raises the possibility that fitness is compromised when co-evolved mitochondrial and nuclear alleles are separated during hybridization, and that paternal mitotypes that do enter the oocyte at fertilization might improve individual fitness. Subsequent selection for individuals with increasing levels of the paternal mitotype might eventually lead to homoplasmy for the paternal mitotype in the presence of the paternal nuclear background. While our data suggest that this process occurs over only several generations, future efforts will focus on better understanding the tempo of paternal mitochondrial transmission and the identification of loci involved in facilitating hybrid paternal mitochondrial transmission. This information will be useful in understanding the evolution of uniparental mitochondrial transmission.
