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Auger, R.

Publications and source records attributed to Auger, R..

2 recordsLinked to original sources

Polysaccharide release factors drive lipid-carrier recycling in bacteria

Gram-negative bacteria build their cell envelope by transporting various sugar-based precursors across the inner membrane on the shared lipid carrier undecaprenyl (also known as C55). Because the cellular pool of undecaprenyl is finite and used by multiple competing pathways, it must be efficiently regenerated to sustain envelope assembly. Yet the enzymes that release polysaccharide cargo from the lipid carrier have remained elusive, leaving a major gap in our understanding of bacterial envelope biogenesis. Here we identify three periplasmic enzymes in Escherichia coli - UprA, UprB, and UprC - that hydrolyze the bond linking polysaccharide precursors to undecaprenyl. UprA releases elongating peptidoglycan glycan strands from the inner membrane, catalyzing the long-sought terminal step of peptidoglycan synthesis. UprB cleaves the undecaprenyl-linked initiating unit common to the enterobacterial common antigen and O-antigen pathways, while UprC is the likely release factor for the colanic acid pathway. These enzymes define a widespread Upr-like protein family (formerly DUF218) as polysaccharide release factors, revealing a unifying mechanism by which bacteria coordinate envelope assembly. Because all three Upr-like proteins share a conserved catalytic core, this family represents a potential target for antibiotics that simultaneously disrupt multiple envelope pathways.

microbiology↗

Mechanistic insights into Enterocin C targeting the undecaprenyl phosphate recycling protein BacA

Enterococcus faecalis is an important opportunistic pathogen responsible for healthcare-associated infections. It is intrinsically resistant to various antibiotics, particularly to cephalosporins and vancomycin, creating an urgent need for alternative therapeutics. In this context, bacteriocins warrant investigations as a potential source of medical-use antibiotics. Herein, we demonstrate that Enterocin C, a class IIb two-peptide bacteriocin, specifically targets the membrane embedded undecaprenyl phosphate recycling protein BacA from enterococci as a cell surface receptor. Using biochemical and biophysical methods, supported by AlphaFold2 modelling and mutagenesis, we deciphered the EntCs molecular interaction pattern with its target, marking the first mechanistic insight of a two-peptide bacteriocin. The two peptides act cooperatively at nanomolar concentrations to interact with the outward-open catalytic pocket of BacA: the peptide EntC1 docks deeply into the catalytic site, inhibits BacAs enzymatic activity and enables the binding of peptide EntC2, eliciting membrane permeabilization, eventually leading to cell death. A comparative analysis with LcnG, a homologous bacteriocin, reveals a conserved interaction pattern, paving the way for bioengineering of these bacteriocins and developing tailored antimicrobial strategies.

biochemistry↗