Hynes M J
J Bacteriol. 1977 Sep;131(3):770-5. doi: 10.1128/jb.131.3.770-775.1977.
Growth tests and enzyme determinations strongly suggest that the acetamidase of Aspergillus nidulans is induced by a product of acetate metabolism rather than the substrate, acetamide. The cis-dominant mutation, amdI9, which is closely linked to amdS, the structural gene for the acetamidase, results in greatly increased sensitivity to induction by acetate metabolism. Propionate, L-threonine, and ethanol also result in acetamidase induction. Mutations in the facA, facB, and facC genes, which lead to low levels of acetyl-coenzyme A synthase, are epistatic to the amdI9 mutation for strong growth on acetamide medium and abolish acetamide and propionamide induction of the acetamidase and isocitrate lyase enzymes. Acetate, L-threonine, and ethanol, however, can induce these enzymes in strains containing facA and facC lesions but not in strains containing a facB lesion. The evidence suggests that acetamidase and isocitrate lyase may be induced by a similar mechanism.
生长试验和酶活性测定有力地表明,构巢曲霉的乙酰胺酶是由乙酸代谢产物而非底物乙酰胺诱导产生的。与乙酰胺酶结构基因amdS紧密连锁的顺式显性突变amdI9,导致对乙酸代谢诱导的敏感性大大增加。丙酸盐、L-苏氨酸和乙醇也会导致乙酰胺酶的诱导。facA、facB和facC基因的突变会导致乙酰辅酶A合成酶水平降低,这些突变对于在乙酰胺培养基上的强劲生长而言,对amdI9突变具有上位性,并消除乙酰胺和丙酰胺对乙酰胺酶和异柠檬酸裂解酶的诱导作用。然而,乙酸、L-苏氨酸和乙醇可以在含有facA和facC损伤的菌株中诱导这些酶,但在含有facB损伤的菌株中则不能。有证据表明,乙酰胺酶和异柠檬酸裂解酶可能通过类似的机制被诱导。