Characterization of colicin M and its orthologs targeting bacterial cell wall peptidoglycan biosynthesis

Microb Drug Resist. 2012 Jun;18(3):222-9. doi: 10.1089/mdr.2011.0230. Epub 2012 Mar 20.

Abstract

For a long time, colicin M was known for killing susceptible Escherichia coli cells by interfering with cell wall peptidoglycan biosynthesis, but its precise mode of action was only recently elucidated: this bacterial toxin was demonstrated to be an enzyme that catalyzes the specific degradation of peptidoglycan lipid intermediate II, thereby provoking the arrest of peptidoglycan synthesis and cell lysis. The discovery of this activity renewed the interest in this colicin and opened the way for biochemical and structural analyses of this new class of enzyme (phosphoesterase). The identification of a few orthologs produced by pathogenic strains of Pseudomonas further enlarged the field of investigation. The present article aims at reviewing recently acquired knowledge on the biology of this small family of bacteriocins.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Bacteriocins / metabolism*
  • Bacteriocins / pharmacology
  • Cell Wall / chemistry
  • Cell Wall / metabolism*
  • Colicins / metabolism*
  • Colicins / pharmacology
  • Escherichia coli / drug effects
  • Escherichia coli / growth & development
  • Models, Molecular
  • Peptidoglycan / biosynthesis*
  • Protein Structure, Tertiary
  • Pseudomonas / genetics
  • Pseudomonas / metabolism
  • Substrate Specificity
  • Uridine Diphosphate N-Acetylmuramic Acid / analogs & derivatives*
  • Uridine Diphosphate N-Acetylmuramic Acid / metabolism

Substances

  • Bacteriocins
  • Colicins
  • Peptidoglycan
  • Uridine Diphosphate N-Acetylmuramic Acid
  • muramyl-NAc-(pentapeptide)pyrophosphoryl-undecaprenol