Metallo-β-lactamases withstand low Zn(II) conditions by tuning metal-ligand interactions

Nat Chem Biol. 2012 Aug;8(8):698-700. doi: 10.1038/nchembio.1005. Epub 2012 Jun 24.

Abstract

A number of multiresistant bacterial pathogens inactivate antibiotics by producing Zn(II)-dependent β-lactamases. We show that metal uptake leading to an active dinuclear enzyme in the periplasmic space of Gram-negative bacteria is ensured by a cysteine residue, an unusual metal ligand in oxidizing environments. Kinetic, structural and affinity data show that such Zn(II)-cysteine interaction is an adaptive trait that tunes the metal binding affinity, thus enabling antibiotic resistance at restrictive Zn(II) concentrations.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptation, Physiological
  • Anti-Bacterial Agents / pharmacology
  • Drug Design
  • Drug Resistance, Bacterial
  • Ligands
  • Models, Molecular
  • Oxidation-Reduction
  • Periplasm
  • Protein Binding
  • Protein Conformation
  • Zinc / chemistry
  • Zinc / metabolism*
  • beta-Lactamases / genetics
  • beta-Lactamases / metabolism*

Substances

  • Anti-Bacterial Agents
  • Ligands
  • beta-Lactamases
  • Zinc