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Gene Review:

vncS - histidine kinase VncS

Streptococcus pneumoniae R6

Robertson, G.T. et al., Mitchell, L.S. et al., Lewis, K., Novak, R. et al.

Lewis,

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Disease relevance of vncS

Experimental meningitis caused by the vncS mutant failed to respond to vancomycin [1].
Deletion of vncS inhibits autolysis and also decreases killing by unrelated antibiotics [2].

High impact information on vncS

Thus, this tolerance effect resulted from changes in cell growth or other erythromycin-dependent phenomena and not inactivation of vncS per se [3].
A model was advanced proposing that the tolerance phenotype resulted from the inability of a vncS mutant to respond to the Vex-transported Pep27 "death peptide" signal and dephosphorylate VncR, thereby preventing relief of repression of autolytic and other cell death functions in response to antibiotics [3].
Although several genes contributing to antibiotic tolerance among pneumococci have been identified, those important in the clinical arena thus far are in a single gene cluster, vex/pep27/vncS/vncR [4].

References

Emergence of vancomycin tolerance in Streptococcus pneumoniae. Novak, R., Henriques, B., Charpentier, E., Normark, S., Tuomanen, E. Nature (1999) [Pubmed]
Programmed death in bacteria. Lewis, K. Microbiol. Mol. Biol. Rev. (2000) [Pubmed]
Vancomycin tolerance induced by erythromycin but not by loss of vncRS, vex3, or pep27 function in Streptococcus pneumoniae. Robertson, G.T., Zhao, J., Desai, B.V., Coleman, W.H., Nicas, T.I., Gilmour, R., Grinius, L., Morrison, D.A., Winkler, M.E. J. Bacteriol. (2002) [Pubmed]
Molecular analysis of antibiotic tolerance in pneumococci. Mitchell, L.S., Tuomanen, E.I. Int. J. Med. Microbiol. (2002) [Pubmed]

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