Evaluation of Gyp7 Protein Ability to Coordinate and Regulate Mitochondrial Genomes Stability

Abstract

Cellular creation of adenosine triphosphate, ATP, is essential for eukaryotic cells to function properly. The ATP molecule drives most of the biochemical and metabolic pathways of the cell. The cell's ATP is produced in the mitochondria. Mutations within the genome of the mitochondria will alter the cell's ability to generate A TP. Preliminary work has shown that loss of the Gyp 7p in Saccharomyces cerevisiae blocks the ability of mitochondria to properly function. The Gyp 7 gene was isolated using a technique called two-hybrid analysis with a known mitochondrial protein called llvSp, which was used as 'bait'. We have shown that a deletion of the Gyp7 gene is not essential for cellular viability in S. cerevisiae. We observed that loss of Gyp 7 decreases both the occurrence of point mutations at microsatellite sequences as well as decreasing the rate at which recombination between direct-repeat DNA sequences occurs. This contributes to the effective that cellular respiration mutation rate increase when Gyp7p is removed. Gyp7 encodes for the production of the GTPase-activating protein (GAP) Gyp7p within the Ypt/Rab transport GTPase pathway. This pathway is involved in protein trafficking within the cell.