The nitrogen metabolite repression system of Aspergillus nidulans allows the expression of genes required for the utilisation of non8208;preferred nitrogen sources to occur only in the absence of the preferred ammonium or glutamine. The transcriptional activation ability of the primary positive regulator of this system, AreA, is modulated through many processes including differential areA mRNA stability, regulation of nuclear import/export and competitive binding with the negative acting AreB. AreA function is also modulated by interaction with the co8208; repressor NmrA and co8208;activator TamA. The co8208;repressor NmrA is able to bind to the GATA Zinc8208;Finger DNA binding region of AreA, but in vivo experiments have shown that this binding is not preferential to AreA binding to GATA containing DNA, so the exact mechanism with which NmrA represses the activity of AreA is unknown. This study aims to investigate this interaction with and repression of AreA through a mutagenic approach. Since overexpression of nmrA can prevent the activity of AreA, resulting in an inability to grow on non8208;preferred nitrogen sources, a screen has been set up to obtain mutants that are insensitive to NmrA activity. The sequence changes in these mutants and the predicted effects on NmrA structure have been determined.
Full conference title:
11 th European Conference on Fungal Genetics
- ECFG 11th (2012)