Abstract
Respiration-deficient mutants can be induced in populations of Saccharomyces growing in the presence of the cysteine antagonist, allyl glycine. Mutations occur, however, only among cells which had been cultivated anaerobically so as to be unadapted to aerobic respiration prior to exposure to the antagonist. The mutagenicity of allyl glycine is relieved by cysteine, and to a lesser extent by homocysteine, methionine, or alpha-amino-n-butyric acid. It is accentuated by homoserine. Evidence is presented indicating that the ability of allyl glycine to induce respiratory mutants is distinct from its general growth-inhibiting properties. It is concluded that the maintenance of the genetic determinant of respiration in Saccharomyces depends upon a particular metabolic function in which cysteine participates. In cells cultivated anaerobically that function is so limited that it can be rendered effectively inactive by growth in the presence of allyl glycine.
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