The molecular basis of vancomycin resistance in clinically relevant Enterococci: crystal structure of D-alanyl-D-lactate ligase (VanA)

Proc Natl Acad Sci U S A. 2000 Aug 1;97(16):8921-5. doi: 10.1073/pnas.150116497.

Abstract

d-alanine-d-lactate ligase from Enterococcus faecium BM4147 is directly responsible for the biosynthesis of alternate cell-wall precursors in bacteria, which are resistant to the glycopeptide antibiotic vancomycin. The crystal structure has been determined with data extending to 2.5-A resolution. This structure shows that the active site has unexpected interactions and is distinct from previous models for d-alanyl-d-lactate ligase mechanistic studies. It appears that the preference of the enzyme for lactate as a ligand over d-alanine could be mediated by electrostatic effects and/or a hydrogen-bonding network, which principally involve His-244. The structure of d-alanyl-d-lactate ligase provides a revised interpretation of the molecular events that lead to vancomycin resistance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bacterial Proteins / chemistry*
  • Carbon-Oxygen Ligases / chemistry*
  • Crystallography, X-Ray
  • Enterococcus faecium / drug effects*
  • Hydrogen Bonding
  • Protein Conformation
  • Vancomycin Resistance*

Substances

  • Bacterial Proteins
  • VanA ligase, Bacteria
  • Carbon-Oxygen Ligases

Associated data

  • PDB/1E4E