Utilization of arginine as a source of nitrogen depends on the presence and inducibility of two arginine catabolic enzymes: arginase and ornithine aminotransferase (OAT) encoded by agaA and otaA genes, respectively. Both genes are induced by arginine and are under the control of nitrogen metabolite repression system which has been shown to be mediated by AREA general activator. The expression of agaA and otaA is repressed by ammonium. However, in areA600 complete loss-of-function mutant the expression of both genes is fully inducible. This implies that the induction of these genes does not directly or indirectly (by inducer exclusion) depends on AREA activator. Unexpectedly, there is no ammonium repression of agaA and otaA in areA600 mutant. There are two possible explanations of these results: AREA positively regulates a gene coding for a repressor of agaA and otaA, or AREA itself is the repressor of these genes. Nitrogen repression of arginine catabolic genes also depends on the negatively acting factor AREB. Ammonium repression of agaA and otaA is lost in areB403/901 loss-of function mutant and is only partial in areB7 mutant (lack of the dimerization domain) what implies that a homo - or heterodimerization is probably necessary for the full activity of the repressor. Analysis of different areA/areB double mutants suggests that these two GATA factors cooperate in repression of arginine catabolic genes under nitrogen repressing conditions.
Full conference title:
9th EUROPEAN CONFERENCE ON FUNGAL GENETICS
- ECFG 9th (2008)