Cellular creation of adenosine triphosphate, ATP, is essential for any eukaryotic cells to function properly. ATP is the molecule that drives many of the biochemical and metabolic pathways of the cell. Much of the cellís ATP is produced in the mitochondria. Mutations within the genome of the mitochondria will alter the cellís ability to generate ATP. Work in the lab has shown that loss of the GYP7 gene in Saccharomyces cerevisiae blocks the ability of mitochondria to properly function. The GYP7 gene was isolated using a technique called two-hybrid analysis with a known mitochondrial protein called Ilv5p which was used as Ďbaití. We have shown that a deletion of the GYP7 gene is not essential for cellular viability in S. cerevisiae. We observed that loss of GYP7 increases both the occurrence of point mutations at microsatellite sequences as well as recombination between direct-repeat DNA sequences. GYP7 encodes for the production of the GTPase-activating protein (GAP) within the Ypt/Rab transport GTPase pathway. This pathway is involved in protein trafficking within the cell.
|Presenter:||Louis DiDone (Graduate Student)|
|Time:||1:30 pm (Session III)|