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J Biol Chem, Vol. 273, Issue 11, 6367-6372, March 13, 1998
From the Institut de Génétique et Microbiologie,
Université Paris-Sud, URA CNRS D 2225, Centre Universitaire
d'Orsay, Bâtiment 409, F-91405 Orsay Cedex, France
Carbon catabolite repression is mediated in
Aspergillus nidulans by the negative acting protein CreA.
The CreA repressor plays a major role in the control of the expression
of the alc regulon, encoding proteins required for the
ethanol utilization pathway. It represses directly, at the
transcriptional level, the specific transacting gene alcR,
the two structural genes alcA and aldA, and
other alc genes in all physiological growth conditions.
Among the seven putative CreA sites identified in the alcA
promoter region, we have determined the CreA functional targets in AlcR constitutive and derepressed genetic backgrounds. Two different divergent CreA sites, of which one overlaps a functional AlcR inverted
repeat site, are largely responsible for alcA repression. Totally derepressed alcA expression is achieved when these
two CreA sites are disrupted in addition to another single site, which overlaps the functional palindromic induction target. The fact that
derepression is always associated with alcA overexpression is consistent with a competition model between AlcR and CreA for their
cognate targets in the same region of the alcA
promoter.
Our results also indicate that the CreA repressor is necessary and
sufficient for the total repression of the alcA gene.
The CreA Repressor Is the Sole DNA-binding Protein Responsible
for Carbon Catabolite Repression of the alcA Gene in
Aspergillus nidulans via Its Binding to a Couple of
Specific Sites
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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