Abstract
In Escherichia coli, hns mutants lack flagellar motility and display an increase in acid stress resistance. Spontaneous phenotypic revertants showed reversion of both H-NS-controlled phenotypes. In the present study, suppressor mutations were identified in the rcsB gene. In addition to RcsA, our experiments establish that H-NS indirectly controlled the RcsB regulator via repression of RcsD. We also show that RcsB(D56E), mimicking phosphorylated RcsB, interacts with GadE to form a RcsB-P/GadE complex, a general direct regulator of glutamate-, arginine- and lysine-dependent acid resistance pathways. In addition, we showed that H-NS positively affects motility via the flhDC master operon repression by RcsB. This substantiates the central role of RcsB in H-NS-mediated control of motility and acid stress resistance.
2010 Elsevier Masson SAS. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Escherichia coli / genetics
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Escherichia coli / metabolism
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Escherichia coli / physiology*
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Escherichia coli Proteins / genetics
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Escherichia coli Proteins / metabolism*
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Fimbriae Proteins / genetics
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Fimbriae Proteins / metabolism*
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Flagella / genetics*
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Flagella / metabolism
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Gene Expression Regulation, Bacterial*
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Hydrogen-Ion Concentration
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Molecular Sequence Data
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Movement
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Operon
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Phosphorylation
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Phosphotransferases / genetics
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Phosphotransferases / metabolism*
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Regulatory Elements, Transcriptional
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Stress, Physiological*
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Suppression, Genetic
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Trans-Activators / genetics
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Trans-Activators / metabolism
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Transcription Factors / genetics
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Transcription Factors / metabolism*
Substances
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Escherichia coli Proteins
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FimG protein, E coli
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GadE protein, E coli
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RcsB protein, E coli
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Trans-Activators
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Transcription Factors
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flhC protein, E coli
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flhD protein, E coli
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Fimbriae Proteins
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Phosphotransferases
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rcsD protein, E coli