Roles of the<i>Aspergillus nidulans</i>homologues of Tup1 and Ssn6 in chromatin structure and cell viability

Abstract

For three different carbon catabolite repressible promoters, alcA, alcR and the bidirectional promoter prnD-prnB, a deletion of rcoA, the Aspergillus nidulans homologue of TUP1, does not result in carbon catabolite derepression. Surprisingly, it results in disruption of the chromatin default structure of alcR and prnD-prnB promoters. In these promoters, and at variance with the wild type, repression occurs in the absence of nucleosome positioning. For alcR, repression occurs together with a nucleosome pattern identical to that found under conditions of full expression, and for prnD-prnB it occurs with a novel pattern that does not correspond to the pattern seen under conditions of repression in a wild-type strain. Deletion of the putative RcoA partner, SsnF, is lethal in A. nidulans.