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Review
. 2001 Feb;45(2):375-81.
doi: 10.1128/AAC.45.2.375-381.2001.

Regulation of VanA- and VanB-type glycopeptide resistance in enterococci

M Arthur  1 , R Quintiliani Jr
Affiliations
Review

Regulation of VanA- and VanB-type glycopeptide resistance in enterococci

M Arthur et al. Antimicrob Agents Chemother. 2001 Feb.
No abstract available

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Figures

FIG. 1
FIG. 1
Events leading to transcriptional activation of the vanA and vanB gene clusters. The Van sensors contain two trans-membrane segments (TMS) that delineate an external loop (EL). The sequence of these regions of VanS and VanSB are not related, as is found for sensors that recognize different signals (25). A linker connects the membrane-associated domain to the catalytic cytoplasmic domain (hatched). The catalytic domain is conserved in all sensors and contains a conserved histidine residue (H) which is autophosphorylated. The phosphoryl group (P) is then transferred to an aspartate residue (D) of the effector domain of VanR or VanRB. The effector domain is also conserved in all response regulators (25). Phosphorylation of the effector domain activates the DNA binding domain leading to increased affinity for the regulatory regions of the target promoters. The DNA binding domains of VanR and VanRB are related to those of response regulators belonging to the OmpR subfamily (25).
FIG. 2
FIG. 2
Regulation of the PR and PH promoters. (A) Schematic representation of the vanA gene cluster showing details of the regulatory region of PR and PH. An amplification loop results from binding of phospho-VanR to PR, increased transcription of vanR, and accumulation of phospho-VanR following phosphorylation (4). (B) Determination of the effective concentrations of phospho-VanR and VanR required to saturate at 50% (EC50) DNA fragments carrying the PR and PH promoters based on gel shift experiments indicated that phosphorylation increases the affinity of the response regulator for DNA at both promoters and that the affinity is higher for PH than for PR (26). In spite of these differences, the PR and PH promoters were found to be coordinately regulated in vivo (C) and to have a similar strength (5).
See this image and copyright information in PMC

References

    1. Allen N E, Hobbs J N., Jr Induction of vancomycin resistance in Enterococcus faecium by non-glycopeptide antibiotics. FEMS Microbiol Lett. 1995;132:107–114. - PubMed
    1. Al-Obeid S, Billot-Klein D, Van Heijenoort J, Collatz E, Gutmann L. Replacement of the essential penicillin-binding protein 5 by high-molecular mass PBPs may explain vancomycin-β-lactam synergy in low-level vancomycin-resistant Enterococcus faecium D366. FEMS Microbiol Lett. 1992;91:79–84. - PubMed
    1. Arthur M, Depardieu F, Cabanie L, Reynolds P, Courvalin P. Requirement of the VanY and VanX d, d-peptidases for glycopeptide resistance in enterococci. Mol Microbiol. 1998;30:819–830. - PubMed
    1. Arthur M, Depardieu F, Courvalin P. Regulated interactions between partner and non-partner sensors and response regulators that control glycopeptide resistance gene expression in enterococci. Microbiology. 1999;145:1849–1858. - PubMed
    1. Arthur M, Depardieu F, Gerbaud G, Galimand M, Leclereq R, Courvalin P. The VanS sensor negatively controls VanR-mediated transcriptional activation of glycopeptide resistance genes of Tn1546 and related elements in the absence of induction. J Bacteriol. 1997;179:97–106. - PMC - PubMed