Induction of respiratory deficiency by repression of the respiratory system in a mutant of Saccharomyces cerevisiae

Abstract

Cells of a mutant strain of Saccharomyces cerevisiae produce daughter cells with respiratory deficiency of the cytoplasmic petite type when growing under conditions of respiratory repression, that is, in the presence of glucose or under anoxia, but otherwise produce respiratory normal cultures. Apart from inheriting the repressionpetite induction character, the latter are normal in other respects such as response to specific mutagens and oxygen uptake under different physiological conditions. Chloramphenicol, although specifically inhibiting the synthesis of mitochondriabound cytochromes in this strain, does not induce the petite mutation in cultures growing on a non-repressing sugar. The character of anoxia or glucose induction ( gi) of petite appears to be under the control of a recessive nuclear gene and spontaneous reversion to normal takes place with a low frequency. Since petite cells show effective loss of mitochondrial DNA, these results are believed to provide evidence that the replication and/or transmission of the mitochondrial genetic information under respiratory repression is controlled by a system distinct from that operating under respiratory adaptation. In the latter, genetic continuity is probably achieved by auto-reproduction and passive inheritance of intact mitochondria—a mechanism not affected by chloramphenicol, while the former system is dependent on the induced activity of a nuclear gene or genes.