The relationship between respiratory deficiency and suppressiveness in yeast as determined with segregational mutants.

HE development of a normal respiratory phenotype in yeast requires the Tpresence of an autoreproducing and presumably particulate cytoplasmic factor present in normal yeast and lost or functionally inactivated in the so-called respiration-deficient vegetative mutants (“vegetative petites”). This was inferred from the nontransmission of the respiratory deficiency to the sexual progeny in crosses of the neutral vegetative mutants with normal yeast ( EPHRUSSI, HOTTINGUER and TAVLITZKI 1949; EPHRUSSI, DE MARGERIE-HOTTINGUER and OMAN 1955) and confirmed by the study of heterokaryons (WRIGHT and LEDERBERG 1957). It is now known that the majority of cytoplasmic mutants are suppressive, i.e.. when crossed with normal yeast, they impose their respiratory phenotype on a fraction of the zygotes and/or the vegetative progeny of the zygotes (EPHRUSSI, DE MARGERIE-HOTTINGUER and OMAN 1955). Vegetative mutants of independent origin differ in the degree of this interference with the maintenance or development of the respiratory ability: they are said to possess different “degrees of suppressiveness,” reflected in, and measured by, the fraction of zygotes which give rise to respiration-deficient clones. The various degrees of suppressiveness exhibit considerable stability during the vegetative proliferation of cytoplasmic mutants ( EPHRUSSI and GRANDCHAMP 1962). While the transmission of the respiratory deficiency of vegetative mutants is always cytoplasmic, little is known about the inheritance of the different degrees of suppressiveness. In other words, the genetic determination of suppressiveness and of its variations is unknown. One may wonder whether the suppressive property of the mutants under consideration is a consequence of (1 ) the lack of respiration, or (2) the “loss” of the normal cytoplasmic factor, or ( 3 ) the presence of a competing factor which, on the simplest hypothesis, could be the functionally inactive normal factor itself. Some of these questions can be answered by the study of the suppressiveness of mutants which owe their respiratory deficiency to gene mutations and which do or do not contain the normal cytoplasmic factor (referred to as “segregational”