Biochemical and genetic characterization of respiration-deficient mutants of Chinese hamster cells with a Gal- phenotype.

Abstract

Four Chinese hamster somatic cell mutants A13G9, 34A13G32, 2A13G14, and V6IG15 with a Gal- phenotype have the following characteristics: (1) a low respiration rate; (2) a reduced Krebs cycle activity; (3) a low level of stimulation of oxygen consumption of mutant mitochondria by malate; (4) an absolute dependence on an ample supply of glucose to sustain a high rate of glycolysis; (5) a defect in the electron transport chain from NADH to coenzyme Q; and (6) no appreciable activity of rotenone-sensitive NADH oxidase in mutant mitochondria. These four mutants and another mutant, P12GX1, were analyzed by complementation analysis using seven other respiratory mutants of Dr. Scheffler which define seven complementation groups (I-VII). P12GX1 fails to complement mutant CCL16-B9 (group IV). A13G9 and 34A13G32 do not complement each other. Mutants V6IG15, A13G9, and 34A13G32 define two new groups of complementation (VIII and IX), while 2A13G14 does not complement mutants of groups II and VI.