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Biotecnologia Aplicada
Elfos Scientiae
ISSN: 0684-4551
Vol. 13, Num. 3, 1996, pp. 212
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Biotecnologia Aplicada 1996 Volume 13 No. 3,
pp.212
CARBON CATABOLITE REPRESSION IN Aspergillus nidulans
Beatriz Cubero, Martine Mathieu, Ramon Gonzalez, Dennis Gomez,
Victoria Gavrias, Cristina Panozzo, Beatrice Felenbok and
Claudio Scazzocchio
Institut de Genetique et Microbiologie, Universite Paris Sud,
91405, Orsay, France.
Code Number:BA96090
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Carbon catabolite repression is mediated in Aspergillus
nidulans by the product of the negative acting gene creA.
We have studied in detail the mechanism of repression in two
systems. The ethanol regulon is subject to specific induction
and carbon cataboline repression. The proline utilization gene
cluster is subject to these two forms of control but also to
nitrogen metabolite repression.
Repression of the ethanol regulon is independent of the
nitrogen source, on the other hand, repression of the proline
gene cluster is only achieved when both a nitrogen and
repressing carbon source are present. Repression of the
proline gene cluster acts directly on the structural genes,
repression of the specific regulatory gene is marginal and of
no physiological significance.
The ethanol regulon is controlled by a double lock mechanism,
drastic repression of the specific, positive-acting regulatory
gene and direct repression of the structural genes. We have
carried a limited mutational analysis of the creA gene. We
have identified mutations on the promoter, in the DNA binding
domain and in the carboxy-terminus of the protein. The binding
sites have been determined in vitro. The consensus
sequence recognized by the creA Zn fingers is 5'SYGGRG3'.
Classical and reverse genetical experiments have been carried
out to determine, among a multitude of sites, those which are
of physiological importance.
The data shows that creA acts in rather different ways in the
two systems. In the ethanol regulon it prevents the binding of
or activation by the positively-acting, specific alcR protein.
This mechanism acts both on expression of the alcR gene itself
and of the structural gene alcA. In the proline cluster it
acts by preventing the activity of a different, and possibly
general transcription factor. This explains the particular
interaction of carbon and nitrogen metabolite repression found
in this system. The site of action of this new factor has been
narrowed down to 600 bp in the intergenic region between the
divergently transcribed prnD (proline oxidase) and prnB
(proline permease) genes. The creA protein does not prevent
directly the binding of this new, positive acting,
transcription factor.
Copyright 1996 Elfos Scientiae
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