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Journal of Bacteriology, February 2006, p. 1381-1388, Vol. 188, No. 4
0021-9193/06/$08.00+0     doi:10.1128/JB.188.4.1381-1388.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Characterization of Late Acyltransferase Genes of Yersinia pestis and Their Role in Temperature-Dependent Lipid A Variation

Roberto Rebeil,1,{dagger} Robert K. Ernst,2 Clayton O. Jarrett,1 Kristin N. Adams,2 Samuel I. Miller,2,3,4 and B. Joseph Hinnebusch1*

Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840,1 Departments of Medicine,2 Microbiology,3 Genome Sciences, University of Washington, Seattle, Washington 981954

Received 14 October 2005/ Accepted 27 November 2005

Yersinia pestis is an important human pathogen that is maintained in flea-rodent enzootic cycles in many parts of the world. During its life cycle, Y. pestis senses host-specific environmental cues such as temperature and regulates gene expression appropriately to adapt to the insect or mammalian host. For example, Y. pestis synthesizes different forms of lipid A when grown at temperatures corresponding to the in vivo environments of the mammalian host and the flea vector. At 37°C, tetra-acylated lipid A is the major form; but at 26°C or below, hexa-acylated lipid A predominates. In this study, we show that the Y. pestis msbB (lpxM) and lpxP homologs encode the acyltransferases that add C12 and C16:1 groups, respectively, to lipid IVA to generate the hexa-acylated form, and that their expression is upregulated at 21°C in vitro and in the flea midgut. A Y. pestis {Delta}msbB {Delta}lpxP double mutant that did not produce hexa-acylated lipid A was more sensitive to cecropin A, but not to polymyxin B. This mutant was able to infect and block fleas as well as the parental wild-type strain, indicating that the low-temperature-dependent change to hexa-acylated lipid A synthesis is not required for survival in the flea gut.

* Corresponding author. Mailing address: Laboratory of Human Bacterial Pathogenesis, NIH, NIAID, Rocky Mountain Laboratories, 903 S. 4th St., Hamilton, MT 59840. Phone: (406) 363-9260. Fax: (406) 363-9394. E-mail: jhinnebusch{at}niaid.nih.gov.

{dagger} Present address: Sandia National Laboratory, Albuquerque, NM.

Journal of Bacteriology, February 2006, p. 1381-1388, Vol. 188, No. 4
0021-9193/06/$08.00+0     doi:10.1128/JB.188.4.1381-1388.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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