Mutants affecting histidine utilization in Aspergillus nidulans

Abstract

Wild-type strains of Aspergillus nidulans grow poorly on L-histidine as a sole nitrogen source. The synthesis of the enzyme histidase (EC. 4.3.1.3) appears to be a limiting factor in the growth of the wild type, as strains carrying the mutant areA102 allele have elevated histidase levels and grow strongly on histidine as a sole nitrogen source. L-Histidine is an extremely weak sole carbon source for all strains. Ammonium repression has an important role in the regulation of histidase synthesis and the relief of ammonium repression is dependent on the availability of a good carbon source. The level of histidase synthesis does not respond to the addition of exogenous substrate. Mutants carrying lesions in the sarA or sarB loci (suppressor of areA102) have been isolated. The growth properties of these mutants on histidine as a sole nitrogen source correlate with the levels of histidase synthesized. Mutation at the sarA and sarB loci also reduces the utilization of a number of other nitrogen sources. The data suggest that these two genes may code for regulatory products involved in nitrogen catabolism. No histidase structural gene mutants were identified and possible explanations of this are discussed. © 1975, Cambridge University Press. All rights reserved.