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Applied and Environmental Microbiology, June 2009, p. 3998-4006, Vol. 75, No. 12
0099-2240/09/$08.00+0     doi:10.1128/AEM.02657-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

CpxRA Contributes to Xenorhabdus nematophila Virulence through Regulation of lrhA and Modulation of Insect Immunity{triangledown}

Erin E. Herbert Tran{dagger} 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 is a blood pathogen of insects that requires the CpxRA signal transduction system for full virulence (E. E. Herbert et al., Appl. Environ. Microbiol. 73:7826-7836, 2007). We show here that the {Delta}cpxR1 mutant has altered localization, growth, and immune suppressive activities relative to its wild-type parent during infection of Manduca sexta insects. In contrast to wild-type X. nematophila, which were recovered throughout infection, {Delta}cpxR1 cells did not accumulate in hemolymph until after insect death. In vivo imaging of fluorescently labeled bacteria within live insects showed that {Delta}cpxR1 displayed delayed accumulation and also occasionally were present in isolated nodes rather than systemically throughout the insect as was wild-type X. nematophila. In addition, in contrast to its wild-type parent, the {Delta}cpxR1 mutant elicited transcription of an insect antimicrobial peptide, cecropin. Relative to phosphate-buffered saline-injected insects, cecropin transcript was induced 21-fold more in insects injected with {Delta}cpxR1 and 2-fold more in insects injected with wild-type X. nematophila. These data suggest that the {Delta}cpxR1 mutant has a defect in immune suppression or has an increased propensity to activate M. sexta immunity. CpxR regulates, directly or indirectly, genes known or predicted to be involved in virulence (E. E. Herbert et al., Appl. Environ. Microbiol. 73:7826-7836, 2007), including lrhA, encoding a transcription factor necessary for X. nematophila virulence, motility, and lipase production (G. R. Richards et al., J. Bacteriol. 190:4870-4879, 2008). CpxR positively regulates lrhA transcript, and we have shown that altered regulation of lrhA in the {Delta}cpxR1 mutant causes this strain's virulence defect. The {Delta}cpxR1 mutant expressing lrhA from a constitutive lac promoter showed wild-type virulence in M. sexta. These data suggest that CpxR contributes to X. nematophila virulence through the regulation of lrhA, immune suppression, and growth in Insecta.

* 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

{triangledown} Published ahead of print on 17 April 2009.

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

Applied and Environmental Microbiology, June 2009, p. 3998-4006, Vol. 75, No. 12
0099-2240/09/$08.00+0     doi:10.1128/AEM.02657-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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