Ribosome activity and degradation in meiotic cells of Saccharomyces cerevisiae.

Summary The acetamidase of Aspergillus nidulans is induced by sources of acetyl CoA, benzoate and benzamide and by -alanine and other -amino acids. The effects of these groups of inducers are approximately additive. The cis-acting control site mutant, amdI9, affects induction by sources of acetyl-CoA specifically. Lesions in the amdR and gatA genes affect induction by -amino acids specifically. Mutations in the amdA gene can lead to elevated acetamidase levels which still respond to the various inducers. The induction controls act independently of repression control by nitrogen metabolites and are not altered by the areA102 mutation. The properties of double mutants with lesions affecting the different control mechanisms also indicate their independence of each other. It is suggested that the acetamidase is subject to complex control by multiple regulatory circuits and that functionally independent control sites adjacent to the structural gene occur.