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The large mechanosensitive channel MscL determines bacterial susceptibility to the bacteriocin sublancin 168

Thijs R H M Kouwen1, Erik N Trip, Emma L Denham

  • 1Department of Medical Microbiology, University Medical Center Groningen and University of Groningen, Hanzeplein 1, P.O. Box 30001, 9700 RB Groningen, The Netherlands.

Antimicrobial Agents and Chemotherapy
|September 10, 2009
PubMed

Insights

The large mechanosensitive channel of conductance MscL is crucial for bacterial susceptibility to the lantibiotic sublancin 168. This finding reveals a specific cellular determinant for sublancin 168 action against bacteria like Staphylococcus aureus.

Area of Science:

  • Microbiology
  • Bacteriology
  • Molecular Biology

Background:

  • Sublancin 168 is a stable, broad-spectrum lantibiotic produced by Bacillus subtilis.
  • Its mode of action and cellular targets remain largely unknown, hindering its therapeutic potential.
  • Susceptible organisms include pathogens like Staphylococcus aureus.

Purpose of the Study:

  • To identify cellular factors determining bacterial susceptibility to sublancin 168.
  • To elucidate the mechanism of sublancin 168 action.
  • To investigate the role of specific bacterial components in sublancin 168 resistance.

Main Methods:

  • Growth inhibition and competition assays were performed on Bacillus subtilis and Staphylococcus aureus.
  • Experiments were conducted in liquid cultures and on plates with varying NaCl concentrations.
  • The involvement of the large mechanosensitive channel of conductance (MscL) was assessed.

Main Results:

  • NaCl concentration affected sublancin 168-mediated growth inhibition, lowering susceptibility without altering antibiotic properties.
  • Bacterial susceptibility to sublancin 168 was critically dependent on the presence of MscL.
  • MscL was not involved in susceptibility to other bacteriocins, such as nisin and Pep5.

Conclusions:

  • MscL is a specific determinant of bacterial susceptibility to sublancin 168.
  • MscL may act as a direct target or an entry point for sublancin 168 into the bacterial cytoplasm.
  • These findings provide novel insights into lantibiotic mechanisms and potential resistance factors.

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