Affiliation:
1. Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC), Gif-sur-Yvette, France
Abstract
Overexpression of the chromosomal
cbrA
gene allows
E. coli
to resist colicin M (ColM), a bacteriocin specifically hydrolyzing the undecaprenyl-PP-MurNAc(-pentapeptide)-GlcNAc (lipid II) peptidoglycan precursor of targeted cells. This resistance results from a CbrA-dependent modification of the precursor structure, i.e., reduction of the α-isoprenyl bond of C
55
-carrier lipid moiety that is proximal to ColM cleavage site. This modification, observed here for the first time in eubacteria, annihilates the ColM activity without affecting peptidoglycan biogenesis. These data, which further increase our knowledge of the substrate specificity of this colicin, highlight the capability of
E. coli
to generate reduced forms of C
55
-carrier lipid and its derivatives. Whether the function of this modification is only relevant with respect to ColM resistance is now questioned.
Funder
Agence Nationale de la Recherche
Fondation pour la Recherche Médicale
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
3 articles.
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