
Roles of the Aspergillus nidulans homologues of Tup1 and Ssn6 in chromatin structure and cell viability
Author(s) -
García Irene,
Mathieu Martine,
Nikolaev Igor,
Felenbok Béatrice,
Scazzocchio Claudio
Publication year - 2008
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2008.01379.x
Subject(s) - aspergillus nidulans , catabolite repression , psychological repression , promoter , derepression , chromatin , nucleosome , biology , genetics , microbiology and biotechnology , chemistry , gene , gene expression , mutant
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 .