Genetic analysis of a respiration-deficient mutant of Saccharomyces cerevisiae lacking all cytochromes and accumulating coproporphyrin.

HE cytoplasmic factor ( p ) and many nonallelic chromosomal genes determine the presence of cytochromes in yeast (EPHRUSSI 1953; GUNGE 1966; SHERMAN 1963). Ordinarily, a respiration-deficient (RD) mutant defective in any of these determinants lacks cytochromes a and b, but possesses cytochrome c at a normal or increased level, when grown aerobically. Recently, some mutant yeasts have been reported which have variously altered cytochrome patterns such as decreased amounts of cytochrome c with the normal presence of cytochromes a and b. deficiency in cytochrome a with the presence of cytochromes b and c, etc. (SHERMAN 1964; SHERMAN and SLONIMSKI 1964; SHERMAN 1965). Some pigment presumed to be porphyrin has been noticed. We have previously reported an RD mutant, 5b-1, which lacks all cytochromes and other heme-proteins and accumulates coproporphyrin I11 as the predominant porphyrin, when grown aerobically in yeast extract-peptone glucose medium (SUGIMURA, OKABE, NAGAO and GUNGE 1966). A defect in the conversion of coproporphyrin to protoporphyrin was considered to be the most probable lesion. Strain 5b-1 originated from a pculture of a segregational RD yeast, having the mutant gene p governing inability to grow on nonfermentable carbon source. The P / p corresponds to RJr1 in a previous paper (GUNGE 1966). The question remained unsettled whether the simultaneous loss of all cytochromes was caused by mutations other than that of the chromosomal gene P and the p factor. It was also uncertain whether the loss of all cytochromes and the accumulation of coproporphyrin were coincidental. The present study was designed to clarify these points. The results led to the conclusion that the loss of all cytochromes and the coproporphyrin-accumulation both resulted from a mutation in a single chromosomal gene. The problem of phenotypic reversion to wild type in this mutant is also dealt with, and discussed in relation to the temperature sensitivity of phenotypic expression.