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Carbon catabolite repression of the Aspergillus nidulans xlnA gene
Author(s) -
Orejas Margarita,
MacCabe Andrew Peter,
Pérez González José Antonio,
Kumar Sudeep,
Ramón Daniel
Publication year - 1999
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.1999.01157.x
Subject(s) - catabolite repression , aspergillus nidulans , biology , psychological repression , mutant , gene , biochemistry , fungal protein , reporter gene , xylose , gene expression , fermentation
Expression of the Aspergillus nidulans 22 kDa endoxylanase gene, xlnA , is controlled by at least three mechanisms: specific induction by xylan or xylose; carbon catabolite repression (CCR); and regulation by ambient pH. Deletion analysis of xlnA upstream sequences has identified two positively acting regions: one that mediates specific induction by xylose; and another that mediates the influence of ambient pH and contains two PacC consensus binding sites. The extreme derepressed mutation creA d 30 results in considerable, although not total, loss of xlnA glucose repressibility, indicating a major role for CreA in its CCR. Three consensus CreA binding sites are present upstream of the structural gene. Point mutational analysis using reporter constructs has identified a single site, xlnA .C1, that is responsible for direct CreA repression in vivo . Using the creA d 30 derepressed mutant background, our results indicate the existence of indirect repression by CreA.

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