Open AccessTranscriptome analysis of the Mg 2+ ‐responsive PhoP regulator in Yersinia pestis ⋆
Author(s) -
Zhou Dongsheng,
Han Yanping,
Qin Long,
Chen Zeliang,
Qiu Jingfu,
Song Yajun,
Li Bei,
Wang Jin,
Guo Zhaobiao,
Du Zongmin,
Wang Xiaoyi,
Yang Ruifu
Publication year - 2005
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1016/j.femsle.2005.06.053
Subject(s) - yersinia pestis , mutant , microbiology and biotechnology , biology , regulon , chemistry , gene , virulence , biochemistry
PhoP was previously shown to be important for Yersinia pestis survival in macrophage and under macrophage‐induced stresses. In this work, a phoP disruptant of Y. pestis 201 was generated using the Red cloning procedure. The transcription profile of the wild‐type Y. pestis was then compared with that of the phoP mutant under Mg 2+ ‐limiting conditions. It was revealed that PhoP/PhoQ governed a wide set of cellular pathways in Y. pestis , especially including the positive regulation of many metabolic processes, Mg 2+ transport, peptidoglycan remodeling, lipopolysaccharide (LPS) modification and various stress‐protective functions. The Mg 2+ transport system regulated by PhoP may make Y. pestis to maintain the magnesium homeostasis under low Mg 2+ environments. The PhoP‐controlled stress‐protective functions likely constitute the molecular basis for the observation that mutation of the phoP gene rendered the bacteria more sensitive to various macrophage‐induced stresses. Modification of LPS mediated by PhoP is hypothesized to not only neutralize negative charges as normally done by Mg 2+ ions, but also mediate the resistance of Y. pestis to antimicrobial peptides. The microarray results provide a population of candidate genes or pathways, and further biochemical experiments are needed to elucidate the PhoP‐dependent mechanisms by which Y. pestis survives the antibacterial strategies employed by host macrophages.