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MccE provides resistance to protein synthesis inhibitor microcin C by acetylating the processed form of the

Maria Novikova1, Teymur Kazakov, Gaston H Vondenhoff

  • 1Institute of Gene Biology, Russian Academy of Sciences, Moscow 119334, Russia.

The Journal of Biological Chemistry
|February 18, 2010
PubMed

Insights

Microcin C (McC) normally inhibits bacterial growth. A gene product, MccE, detoxifies processed McC and confers resistance to other toxins like albomycin by acetylation.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Bacterial Toxin Research

Background:

  • Microcin C (McC) is a heptapeptide-nucleotide antibiotic inhibiting enteric bacteria.
  • Processed McC inside producer cells inhibits translation by targeting aspartyl-tRNA synthetase.
  • Understanding McC resistance mechanisms is crucial for controlling bacterial infections.

Purpose of the Study:

  • To investigate the role of the mccE gene product in microcin C (McC) resistance.
  • To elucidate the mechanism by which MccE confers resistance to toxic compounds.
  • To explore the broader implications of MccE in cellular detoxification.

Main Methods:

  • Genetic analysis of the microcin C biosynthetic cluster.
  • Biochemical assays to determine the enzymatic activity of MccE.
  • Resistance assays in Escherichia coli strains.

Main Results:

  • The mccE gene product acetylates processed microcin C (McC), rendering it non-toxic.
  • MccE confers resistance to albomycin, an unrelated inhibitor of seryl-tRNA synthetase.
  • Acetylation by MccE prevents translation inhibition and bacterial growth cessation.

Conclusions:

  • MccE acts as a cellular defense mechanism against toxic aminoacyl-nucleotides.
  • This acetylation pathway may represent a general detoxification strategy for related compounds.
  • MccE and similar enzymes offer potential targets for novel antibacterial strategies.

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