Nitrogen metabolite repression in Aspergillus nidulans: A farewell to tamA?

Abstract

Previous work has established that nitrogen metabolite repression in Aspergillus nidulans is mediated by the positive acting regulatory gene areA. Pateman and Kinghorn (1977) proposed that the gene tamA plays an equally important regulatory role in nitrogen metabolite repression as the result of work with "tamA(r)-50," an "allele" leading to inability to utilise nitrogen sources other than ammonium, and "tamA(d)-1," an "allele" leading to nitrogen metabolite derepression. Both "tamA(r)-50" and "tamA(d)-1" were subsequently lost. We have therefore attempted to reconstruct Pateman and Kinghorn's work with tamA. We propose that "tamA(r)-50" was in fact a pyroB(-) tamA(-) double mutation. pyroB(-) mutations lead to a block in vitamin B6 biosynthesis which can be supplemented by extremely high concentrations of ammonium. tamA(-) mutations, possibly as the result of a membrane alteration, reduce the concentration of ammonium required to supplement the pyroB(-) auxotrophy. There is, however, no evidence that pyroB(-) or tamA- mutations, alone or in combination, affect the regulation of the levels of a number of enzymes subject to nitrogen metabolite repression. Reversion of pyroB(-) strains constitutes a powerful positive selection technique for obtaining a wide variety of mutations in glnA, the probable structural gene for glutamine synthetase. We suggest that the nitrogen metabolite derepressed phenotype attributed to "tamA(d)-1" might have resulted from an extremely leaky glnA(-) mutation.