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Applied and Environmental Microbiology, June 2009, p. 4007-4014, Vol. 75, No. 12
0099-2240/09/$08.00+0     doi:10.1128/AEM.02658-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

CpxRA Influences Xenorhabdus nematophila Colonization Initiation and Outgrowth in Steinernema carpocapsae Nematodes through Regulation of the nil Locus

Erin E. Herbert Tran, Aaron W. Andersen, and Heidi Goodrich-Blair^*

Department of Bacteriology, University of Wisconsin—Madison, Madison, Wisconsin 53706

Received 19 November 2008/ Accepted 3 April 2009

The gammaproteobacterium Xenorhabdus nematophila mutualistically colonizes an intestinal region of a soil-dwelling nematode and is a blood pathogen of insects. The X. nematophila CpxRA two-component regulatory system is necessary for both of these host interactions (E. Herbert et al., Appl. Environ. Microbiol. 73:7826-7836, 2007). Mutualistic association of X. nematophila with its nematode host consists of two stages: initiation, where a small number of bacterial cells establish themselves in the colonization site, and outgrowth, where these cells grow to fill the space. In this study, we show that the Cpx system is necessary for both of these stages. X. nematophila cpxR1 colonized fewer nematodes than its wild-type parent and did not achieve as high a density as did the wild type within a portion of the colonized nematodes. To test whether the cpxR1 host interaction phenotypes are due to its overexpression of mrxA, encoding the type I pilin subunit protein, we assessed the colonization phenotype of a cpxR1 mrxA1 double mutant. This mutant displayed the same colonization defect as cpxR1, indicating that CpxR negative regulation of mrxA does not play a detectable role in X. nematophila-host interactions. CpxR positively regulates expression of nilA, nilB, and nilC genes necessary for nematode colonization. Here we show that the nematode colonization defect of the cpxR1 mutant is rescued by elevating nil gene expression through mutation of nilR, a negative regulator of nilA, nilB, and nilC. These data suggest that the nematode colonization defect previously observed in cpxR1 is caused, at least in part, by altered regulation of nilA, nilB, and nilC.

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* Corresponding author. Mailing address: Department of Bacteriology, University of Wisconsin—Madison, 1550 Linden Dr., Madison, WI 53706. Phone: (608) 265-4537. Fax: (608) 262-9865. E-mail: hgblair{at}bact.wisc.edu

Published ahead of print on 17 April 2009.

Present address: Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.

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Applied and Environmental Microbiology, June 2009, p. 4007-4014, Vol. 75, No. 12
0099-2240/09/$08.00+0     doi:10.1128/AEM.02658-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

This article has been cited by other articles:

• Herbert Tran, E. E., Goodrich-Blair, H. (2009). CpxRA Contributes to Xenorhabdus nematophila Virulence through Regulation of lrhA and Modulation of Insect Immunity. Appl. Environ. Microbiol. 75: 3998-4006 [Abstract] [Full Text]