Abstract
Mutants of Apergillus nidulans with lesions in a gene, areA (formerly called amdT), have been isolated by a variety of different selection methods. The areA mutants show a range of pleiotropic growth responses to a number of compounds as sole nitrogen sources, but are normal in utilization of carbon sources. The levels of two amidase enzymes as well as urease have been investigated in the mutants and have been shown to be affected by this gene. Most of the areA mutants have much lower amidase-specific activities when grown in ammonium-containing medium, compared with mycelium incubated in medium lacking a nitrogen source. Some of the areA mutants do not show derepression of urease upon relief of ammonium repression. The dominance relationships of areA alleles have been investigated in heterozygous diploids, and these studies lend support to the proposal that areA codes for a positively acting regulatory product. One of the new areA alleles is partially dominant to areA+ and areA102. This may be a result of negative complementation or indicate that areA has an additional negative regulatory function. Investigation of various amdR; areA double mutants has led to the conclusion that amdR and areA participate in independent regulatory circuits in the control of acetamide utilization. Studies on an amdRc; areA double mutant indicate that areA is involved in derepression of acetamidase upon relief of ammonium repression.