作者: Paola Bisicchia , Nhat Khai Bui , Christine Aldridge , Waldemar Vollmer , Kevin M. Devine
DOI: 10.1111/J.1365-2958.2011.07684.X
关键词:
摘要: The vancomycin resistance operons from Enterococci, Staphylococci and Actinomycetes encode a VanRS two-component signal transduction system (TCS) suite of enzymes to modify the peptidoglycan biosynthetic precursor lipid II eliminate D-Ala-D-Ala cell. Commingling these regulatory enzymatic activities with host functions has potential significantly impact gene expression cell wall metabolism. Here we report effects individually expressing VanR(B) S(B) TCS VanY(B) WH(B) BX(B) proteins in Bacillus subtilis. confers 2 µg ml(-1) concomitant reduced Van-FL staining leads division defect. In contrast E. faecalis S. aureus, VanS(B) is active B. subtilis without addition. Individual repress increase, respectively, PhoPR regulon genes phosphate-limited state. When vancomycin-resistant cells are exposed elevated levels, mutant strains increased growth dependency on vanY(B) frequently arise. Mutation endogenous Ddl ligase necessary sufficient cause both phenotypes. We discuss how may influence establishment van new bacteria.