Abstract
T1 a mutant yeast lacking three regulatory proteins of F1 F0 ATPase, namely ATPase inhibitor, 9K protein and 15K protein, grew on non-fermentable carbon source at the same rate as normal cells but was less viable when incubated in water. During the incu-bation, the cellular ATP content decreased rapidly in the T1 cells but not in normal cells, and respiration-deficient cells appeared among the T1 cells. The same mutation was also induced in D26 cells lacking only the ATPase inhibitor. Overexpression of the ATPase inhibitor in YC63 cells, which were derived from the D26 strain harboring an expression vector containing the gene of the ATPase inhibitor, prevented the decrease of cellular ATP level and the mutation. Isolated T1 mitochondria exhibited ATP hydrolysis for maintenance of membrane potential when antimycin A was added to the mitochondria suspension, while normal and YC63 mitochondria continued to show low hydrolytic activity and low membrane potential. Thus, it is likely that deletion of the ATPase inhib-itor induces ATPase activity of F1 F0 ATPase to create a dispensable membrane potential under the non-nutritional conditions and that this depletes mitochondrial and cellular ATP. The depletion of mitochondrial ATP in turn leads to occurrence of aberrant DNA in mitochondria.
