Studies of partially repressed mutants at the tamA and areA loci in Aspergillus nidulans

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Abstract
Mutants, designated tamA r, have been isolated on the basis of simultaneous resistance to toxic analogues thiourea, aspartate hydroxamate and chlorate with L-alanine as the sole nitrogen source. tamA r mutants are also resistant to methylammonium. This resistance of tamA r mutants is correlated with partially repressed activity of a number of enzyme and transport systems regulated by ammonium. Furthermore, tamA r mutants have low NADP-glutamate dehydrogenase (NADP-GDH) activity and also efflux ammonium under certain growth conditions. Mutants at the areA locus (areA r) have also been isolated on the basis of resistance to these analogues, with nitrate or L-aspartate as the nitrogen source. These, similar to tamA r lesions, result in resistance to methylammonium and are partially repressed for ammonium repressible systems, but in contrast to tamA r, areA r alleles have wild-type NADP-GDH activity and normal ammonium efflux. tamA r and areA r mutants grow as wild type on all nitrogen or carbon sources tested, are recessive, and appear to be epistatic to all other mutations (gdhA1, meaA8 and meaB6) which result in derepressed levels of ammonium regulated system. Whereas tamA r and areA r phenotypes are additive, tamA r is epistatic to areA d phenotype.