Aspergillus nidulans has at least two permeases for l-proline. The prnB gene of the prn gene cluster specifies the major proline permease, which is inducible by proline. Synthesis of the prnB permease is subject to repression by ammonium at 37 °C but not at 25 °C. A genetically unidentified minor proline permease(s) does not respond to proline induction or ammonium repression but is inhibited by ammonium. areAr mutants are unable to utilize nitrogen sources other than ammonium because they lack a positive-acting regulatory product required for expression of ammonium-repressible activities. However, there are very few cases in which the lack of growth of areAr mutants on a particular nitrogen source can be attributed to a reduction in the level of a particular enzyme activity or permease. Reduced expression of the prnB permease can account for the inability of areAr mutants to utilize proline. This is demonstrated by the ability of cis-acting regulatory mutations designated prnd, which derepress synthesis of the prnB permease, to suppress areAr mutations for proline utilization. The apparent ability of prnd mutations to derepress synthesis of proline oxidase and l-pyrroline-5-carboxylate dehydrogenase is probably an indirect consequence of their ability to derepress synthesis of the prnB permease, preventing inducer exclusion. There is presently no evidence that prnd mutations directly affect expression of the prnA, prnC or prnD genes, but this possibility has not been definitively eliminated.
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