Mitochondrial genome maintenance is essential for the normal function of the cell. Mutations in mitochondrial DNA (mtDNA) lead to the loss of mitochondrial function and have been associated with a variety of human neuromuscular and age-related diseases. S. cerevisiae is a facultative anaerobe that can grow in the absence of respiration under specific growth conditions, although mitochondria are still required for viability. The lab used a yeast two-hybrid assay with the known mitochondrial protein, Ilv5p, to isolate genes involved in the organization, repair, and recombination of mtDNA. The YOL057w gene was identified in this screen. Its product is highly homologous to a human exopeptidase, dipeptidyl peptidase III (DPPIII). A deletion of YOL057w was found to increase the frequency at which yeast cells spontaneously lose the ability to respire. Three different assays were used to determine the molecular mechanism leading to this respiration loss phenotype. We observed that loss of YOL057w protein function led to a 3.5-fold increase in the rate of microsatellite instability, 6-fold decrease in the rate at which spontaneous point mutations occur, and had no affect on the rate of intragenic direct-repeat recombination. A yol057w deletion strain also displays altered mitochondrial structures and genome number.
|Presenters:||Jessica Kerr (Undergraduate Student)
Jonathan Malecki (Undergraduate Student)
|Time:||2 pm (Session III)|