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Infection and Immunity, August 2007, p. 3913-3924, Vol. 75, No. 8
0019-9567/07/$08.00+0     doi:10.1128/IAI.01346-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Extracytoplasmic-Stress-Responsive Pathways Modulate Type III Secretion in Yersinia pseudotuberculosis{triangledown}

Katrin E. Carlsson,1 Junfa Liu,1,2 Petra J. Edqvist,1 and Matthew S. Francis1*

Department of Molecular Biology, Umeå University, SE-901 87 Umeå, Sweden,1 College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, People's Republic of China2

Received 22 August 2006/ Returned for modification 9 October 2006/ Accepted 2 May 2007

Three signal transduction pathways, the two-component systems CpxRA and BaeSR and the alternative sigma factor {sigma}E, respond to extracytoplasmic stress that facilitates bacterial adaptation to changing environments. At least the CpxRA and {sigma}E pathways control the production of protein-folding and degradation factors that counter the effects of protein misfolding in the periplasm. This function also influences the biogenesis of multicomponent extracellular appendages that span the bacterial envelope, such as various forms of pili. Herein, we investigated whether any of these regulatory pathways in the enteropathogen Yersinia pseudotuberculosis affect the functionality of the Ysc-Yop type III secretion system. This is a multicomponent molecular syringe spanning the bacterial envelope used to inject effector proteins directly into eukaryotic cells. Disruption of individual components revealed that the Cpx and {sigma}E pathways are important for Y. pseudotuberculosis type III secretion of Yops (Yersinia outer proteins). In particular, a loss of CpxA, a sensor kinase, reduced levels of structural Ysc (Yersinia secretion) components in bacterial membranes, suggesting that these mutant bacteria are less able to assemble a functional secretion apparatus. Moreover, these bacteria were no longer capable of localizing Yops into the eukaryotic cell interior. In addition, a cpxA lcrQ double mutant engineered to overproduce and secrete Yops was still impaired in intoxicating cells. Thus, the Cpx pathway might mediate multiple influences on bacterium-target cell contact that modulate Yersinia type III secretion-dependent host cell cytotoxicity.

* Corresponding author. Mailing address: Department of Molecular Biology, Umeå University, SE-901 87 Umeå, Sweden. Phone: 46-(0)90-7852536. Fax: 46-(0)90-771420. E-mail: matthew.francis{at}molbiol.umu.se

{triangledown} Published ahead of print on 21 May 2007.

Editor: F. C. Fang

Infection and Immunity, August 2007, p. 3913-3924, Vol. 75, No. 8
0019-9567/07/$08.00+0     doi:10.1128/IAI.01346-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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  • Altman, E., Segal, G. (2008). The Response Regulator CpxR Directly Regulates Expression of Several Legionella pneumophila icm/dot Components as Well as New Translocated Substrates. J. Bacteriol. 190: 1985-1996 [Abstract] [Full Text]  
  • Carlsson, K. E., Liu, J., Edqvist, P. J., Francis, M. S. (2007). Influence of the Cpx Extracytoplasmic-Stress-Responsive Pathway on Yersinia sp.-Eukaryotic Cell Contact. Infect. Immun. 75: 4386-4399 [Abstract] [Full Text]  


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