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Nucleic Acids Res. 2010 Jun;38(11):3546-54. doi: 10.1093/nar/gkq097. Epub 2010 Feb 26.

Acid stress response in Escherichia coli: mechanism of regulation of gadA transcription by RcsB and GadE.

Author information

1
Université de Toulouse, UPS, Laboratoire de Microbiologie et Génétique Moléculaires, F-31000 Toulouse and CNRS, LMGM, F-31000 Toulouse, France. castanie@ibcg.biotoul.fr

Abstract

Escherichia coli can survive extreme acid stress for several hours. The most efficient acid resistance system is based on glutamate decarboxylation by the GadA and GadB decarboxylases and the import of glutamate via the GadC membrane protein. The expression of the corresponding genes is controlled by GadE, the central activator of glutamate-dependent acid resistance (GDAR). We have previously shown by genetic approaches that as well as GadE, the response regulator of the Rcs system, RcsB is absolutely required for control of gadA/BC transcription. In the presence of GadE, basal activity of RcsB stimulates the expression of gadA/BC, whereas activation of RcsB leads to general repression of the gad genes. We report here the results of various in vitro assays that show RcsB to regulate by direct binding to the gadA promoter region. Furthermore, activation of gadA transcription requires a GAD box and binding of an RcsB/GadE heterodimer. In addition, we have identified an RcsB box, which lies just upstream of the -10 element of gadA promoter and is involved in repression of this operon.

PMID:
20189963
PMCID:
PMC2887963
DOI:
10.1093/nar/gkq097
[Indexed for MEDLINE]
Free PMC Article

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