Abstract
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.
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