Carbon catabolite repression of the Aspergillus nidulans xlnA gene

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 actin...

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Bibliographic Details
Published in:Molecular microbiology 1999-01, Vol.31 (1), p.177-184
Main Authors: Orejas, Margarita, MacCabe, Andrew Peter, Pérez González, José Antonio, Kumar, Sudeep, Ramón, Daniel
Format: Article
Language:English
Subjects:
Aspergillus nidulans
Aspergillus nidulans - enzymology
Aspergillus nidulans - genetics
Binding Sites
Carbon - metabolism
Endo-1,4-beta Xylanases
Fungal Proteins - genetics
Fungal Proteins - metabolism
Fungal Proteins - physiology
Gene Expression Regulation, Enzymologic
Gene Expression Regulation, Fungal
Glucose - metabolism
Glutathione Transferase - genetics
Glutathione Transferase - metabolism
Mutagenesis, Site-Directed
Promoter Regions, Genetic
Recombinant Fusion Proteins - genetics
Recombinant Fusion Proteins - metabolism
Recombinant Fusion Proteins - physiology
Repressor Proteins - genetics
Repressor Proteins - metabolism
Repressor Proteins - physiology
Xylosidases - genetics
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Summary: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 creAd30 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 creAd30 derepressed mutant background, our results indicate the existence of indirect repression by CreA.
ISSN:0950-382X
1365-2958
DOI:10.1046/j.1365-2958.1999.01157.x