The vanG glycopeptide resistance operon from Enterococcus faecalis revisited.

摘要: Acquired VanG-type resistance to vancomycin (MIC = 16 μg ml - 1 ) but susceptibility teicoplanin in Enterococcus faecalis BM4518 and WCH9 is due the inducible synthesis of peptidoglycan precursors ending D-alanine-D-serine. The vanG cluster, assigned a chromosomal location, was composed genes recruited from various van operons. 3' end encoded VanG, D-Ala:D-Ser ligase, VanXY G , putative bifunctional D,D-peptidase VanT serine racemase: VanG were implicated as VanC- VanE-type strains. Upstream structural for these proteins vanW with unknown function Y containing frameshift mutation which resulted premature termination protein accounted lack UDP-MurNAc-tetrapeptide cytoplasm. Without mutation, VanY had homology Zn 2 + dependent D,D-carboxypeptidases.The 5' gene cluster contained three vanU vanR vanS encoding regulatory system, co-transcribed constitutively PY promoter, whereas transcription vanY ,W ,G,XY ,T Inducible initiated P promoter. Transfer glycopeptide E. faecalls JH2-2 associated movement, chromosome chromosome, genetic elements c. 240 kb carrying also ermB-encoded erythromycin resistance. Sequence determination flanking regions donor transconjugants revealed same 4 bp direct repeats 22 imperfect inverted that delineated large element.