Emma Johnson

emmajohnsonmail.fresnostate.edu

Mitochondria are commonly known as the powerhouses of the cell and function to convert nutrients from outside sources into molecules the body can use for fuel. The electron transport chain (ETC) is how this conversion process is achieved. Despite the critical nature of the function of the ETC, each protein subunit is encoded either by the nuclear or the mitochondrial genome. This division of labor establishes the potential for the co-evolution of mitochondrial and nuclear genes. Further, the separation of co-evolved mitochondrial and nuclear genotypes by intra-species hybridization has been suggested to lead to mitochondrial dysfunction, hybrid dysfunction, and speciation. Previous data from the Ross Lab shows that experimental intra-species hybrid lines of Caenorhabditis briggsae exhibit reduced organismal fitness that could be due to mitochondrial dysfunction. However, the molecular and genetic basis for this dysfunction is unclear. I hypothesize that ETC efficiency is reduced in hybrids. To test this hypothesis, I will conduct mitochondrial enzyme assays to assess whether ETC function is compromised in these dysfunctional hybrid lines relative to control strains. I will then use statistical methods to determine whether any differences in enzyme assay data are significant. Identifying a biochemical difference between control and experimental hybrid strains is the first step in understanding the genetic basis of mitochondrial dysfunction, and possibly the process of speciation, in inter-population hybrids.