Experimental results are presented in support of the model previously proposed for specific induction of the synthesis of enzymes for arginine catabolism in Saccharomyces cerevisiae (Wiame, 1971a,b), and its connection with end-product repression of arginine biosynthetic enzymes. The data support the occurrence of negative regulation of metabolism in a eukaryote. Operator regions, one for arginase and another for ornithine transaminase, are identified. The operator mutations are fully constitutive. A mutation compatible with the occurrence of a catabolic repressor, CARGR, leads to partial pleiotropic constitutivity. The connection between the induction process and the repression of biosynthetic enzymes is due to a common receptor of metabolic signals, an ambivalent repressor ARGR endowed with the property of a usual repressor for anabolic enzymes and playing the role of inducer at the level of CARGR; this cascade process simulates a positive control. argR- mutations, by producing defective ARGR, "turn on" anabolic enzyme synthesis and "turn off" the synthesis of catabolic enzymes (Fig. 2). The dual role of ARGR is confirmed by the isolation of a mutation argRIId which, in contrast to the defective properties caused by usual argR- mutations, causes a dominant hyperactivity toward induction of a catabolic enzyme, but retains recessive hypoactivity toward repression of an anabolic enzyme. Such an ambivalent repressor is a function necessary for mutual, balanced exclusion between opposite metabolisms. Many operator constitutive mutations for arginase, cargA+O-, change the level of enzyme to a similar value, thus defining a genetic function. One of these mutations, cargA+Oh, in addition to having unusual genetic behaviour, leads to production of twice as much arginase as cargA+O-. This suggests the existence of another genetic region near the structural gene for this enzyme and an additional regulatory function to be analyzed in a separate paper (Dubois & Wiame, 1978).

• PMID: 357733
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Journal Article

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Dubois E, Hiernaux D, Grennon M, Wiame JM

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