Abstract
ABSTRACTMitochondria are typically maternally inherited. In many species, this transmission pattern is produced by sperm-borne mitochondria being eliminated either from sperm before fertilization or from the embryo after fertilization. In the nematode Caenorhabditis briggsae, repeatedly backcrossing hybrids to genetically diverse males can elicit paternal mitochondrial transmission. Studies of other taxa also suggest that hybridization increases paternal mitochondrial transmission. Thus, hybrid genotypes might disrupt the systems that normally prevent paternal mitochondrial transmission. Given the reliance of a number of genetic analyses on the assumption of purely maternal mitochondrial inheritance, it would be broadly valuable to learn more about the processes embryos employ to prevent sperm-borne mitochondria from persisting in offspring, as well as the circumstances under which paternal transmission might be expected to occur. To quantify the tempo of paternal mitochondrial transmission in hybrids, we assessed the presence of paternal mitotypes in replicate lines at three timepoints spanning fifteen generations. All lines exhibited paternal mitochondrial transmission. However, this heteroplasmy always then resolved to homoplasmy for the maternal mitotype. Additionally, one nuclear locus exhibited allele transmission ratio distortion that might reflect mito-nuclear co-evolution. This study frames the genetic architecture of a hybrid genetic incompatibility that leads to paternal mitochondrial transmission and to a reduction in hybrid fitness.
Publisher
Cold Spring Harbor Laboratory
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