Mitochondria are responsible for generating ATP molecules, which are the energy currency of the cell. Some of the proteins necessary for oxidative phosphorylation are encoded on mitochondrial DNA (mtDNA), which is independent of nuclear DNA. Similar to nuclear DNA, the accumulation of mutations in mtDNA can be detrimental to the host. In humans, mutations that lead to neuromuscular and neurodegenerative diseases that have been implicated to mutations in the mitochondrial genome. However, budding yeast are facultative anaerobes that can survive in the absence of oxidative phosphorylation by undergoing fermentation to meet their energy needs under laboratory growth conditions. For this reason, the lab uses the budding yeast, Saccharomyces cerevisisae, to examine genes that may be involved in mutagenesis of mtDNA. One such gene product is Rad52p, encoded in the nuclear genome. Rad52p is essential for nuclear homologous recombination and double-strand break repair, and thus, has been directly implicated in maintaining the integrity of nuclear DNA. The open reading frame of RAD52 contains a total of five potential start codons that may drive expression. The goal of the lab has been to determine whether one of the first three start codons is responsible for creating a Rad52p isoform that is localized to the mitochondria. Experiments required the creation of site-directed mutations of the various start codons. Cells with these mutations were then tested for their ability to undergo nuclear and mitochondrial homologous recombination events. A mutation in the first RAD52ATG reduces mitochondrial (~ 3-fold) but not nuclear homologous recombination events.
|Presenters:||Hugo Avalos (Undergraduate Student)
Matthew Luther (Undergraduate Student)
Emily Whiteside (Undergraduate Student)
|Time:||1:35 pm (Session III)
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