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. 2018 Dec 13;18:213. doi: 10.1186/s12866-018-1342-1

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 1 — Schematic representation of the vanB gene cluster and single nucleotide variations in M1 and Y7 compared with the vanB gene cluster in BM4661. Expression of the vanB cluster genes is regulated by the two-component regulatory system of VanS_B/VanR_B. In the presence of VAN, the histidine kinase VanS_B senses VAN and activates the transcriptional activator VanR_B. Consequently, the two-component regulatory genes (vanR_B and vanS_B) and the resistance genes (vanY_B, vanW, vanH_B, vanB and vanX_B) are transcribed from the VanR_B-driven promoters PR_B and PY_B, respectively, to mediate the VAN resistance [8]. The arrows indicate the location of nucleotide variations (and resulting amino acid substitutions) identified in the vanB gene cluster of M1/Y7 compared with that of BM4661