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Infect. Immun. doi:10.1128/IAI.01450-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Influence of the Cpx extracytoplasmic stress responsive pathway on Yersinia-eukaryotic cell contact

Department of Molecular Biology, Umeå University, SE-901 87 Umeå, Sweden and College of Veterinary Medicine, Huazhong Agricultural University. Wuhan, 430070, P. R. China

^* To whom correspondence should be addressed. Email: matthew.francis{at}molbiol.umu.se.

	Abstract

The extracytoplasmic stress responsive CpxRA two-component signal transduction pathway allows bacteria to adapt to growth in extreme environments. It controls production of periplasmic protein folding and degradation factors, which aids in the biogenesis of multi-component virulence determinants that span the bacterial envelope. This is true of the Yersinia pseudotuberculosis Ysc-Yop type III secretion system. However, despite utilising a second-site suppressor mutation to restore Yop effector secretion by Yersinia defective in the CpxA sensor kinase, these bacteria poorly translocated Yops into target eukaryotic cells. Investigation of this phenotype herein revealed that expression of genes encoding several surface located adhesins is also influenced by the Cpx pathway. In particular, expression and surface localisation of invasin, an adhesin that engages 1-integrins on the eukaryotic cell surface, is severely restricted by removal of CpxA. This reduces bacterial association with eukaryotic cells, which could be suppressed by the ectopic production of CpxA, Invasin or RovA, a positive activator of inv expression. In turn, these infected eukaryotic cells then became susceptible to intoxication by translocated Yop effectors. In contrast, bacteria harbouring an in-frame deletion of cpxR, encoding the cognate response regulator, displayed an enhanced ability to interact with cell monolayers as well as elevated inv and rovA transcription. This phenotype could be drastically suppressed by providing in trans a wild type copy of cpxR. We propose a mechanism of inv regulation influenced by the direct negative affects of phosphorylated CpxR on inv and rovA transcription. In this fashion, sensing of extracytoplasmic stress by CpxAR contributes to productive Yersinia-eukaryotic cell interactions.

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