Thesis

Quantifying paternal mitochondrial DNA transmission in caenorhabditis briggsae hybrids

In most species, mitochondria are maternally inherited. Work in Caenorhabditis elegans has shown that a cellular surveillance system eliminates sperm-borne mitochondria that enter an oocyte. Such a system might have evolved to prevent heteroplasmy (the presence of multiple mitochondrial genotypes in a cell), which can result in mitochondrial disorders. However, in C. briggsae hybrids, repeatedly backcrossing female hybrids to parental males has been suggested to result in paternal mitochondrial transmission. Observations in other taxa have also shown that hybridization increases paternal mitochondrial transmission, raising the hypothesis that hybrid genotypes cause the surveillance system to malfunction and thus facilitate the increase in paternal transmission. This hybrid dysfunction might occur because of recombination of unknown strain-specific molecular signals of paternal mitochondria and their unknown maternal receptor molecules. My objective was to compare the frequencies of paternal transmission in C. briggsae hybrid and control crosses. In twelve novel hybrid lines, all showed preliminary evidence of paternal mitochondrial DNA, although no firm conclusion can be reached as to whether this occurred via paternal mitochondrial transmission. Future work will be needed to unequivocally demonstrated whether paternal mitochondrial transmission occurs, and then to identify the genetic architecture of the quality control system responsible for paternal mitochondrial elimination.

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