Journal
JOURNAL OF BACTERIOLOGY
Volume 188, Issue 4, Pages 1381-1388Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JB.188.4.1381-1388.2006
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Funding
- Intramural NIH HHS Funding Source: Medline
- NIAID NIH HHS [U54 AI057141, U54 AI057141-010005] Funding Source: Medline
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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 degrees C, tetra-acylated lipid A is the major form; but at 26 degrees 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 C-12 and C-16:1 groups, respectively, to lipid A, to generate the hexa-acylated form, and that their expression is upregulated at 21 degrees 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.
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