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Daptomycin-mediated reorganization of membrane architecture causes mislocalization of essential cell division

Joe Pogliano1, Nicolas Pogliano, Jared A Silverman

  • 1Division of Biological Sciences, University of California, San Diego, California, USA. jpogliano@ucsd.edu

Journal of Bacteriology
|June 5, 2012
PubMed

Insights

Daptomycin antibiotic

Area of Science:

  • Microbiology
  • Cell Biology
  • Antibiotic Research

Background:

  • Daptomycin is a crucial lipopeptide antibiotic for treating Gram-positive bacterial infections, including MRSA.
  • Its precise mechanism of action, particularly its interaction with bacterial cell membranes and walls, remains under investigation.

Purpose of the Study:

  • To visualize and elucidate the direct interaction of daptomycin with the bacterial cell membrane and wall.
  • To clarify the sequence of events following daptomycin's cellular entry and its impact on bacterial viability.

Main Methods:

  • Utilizing fluorescence microscopy to observe daptomycin's effects on Bacillus subtilis.
  • Employing fluorescently labeled daptomycin, cell division protein DivIVA, and peptidoglycan biogenesis reporters.

Main Results:

  • Daptomycin induces membrane distortions preceding cell death by over 30 minutes.
  • These membrane defects recruit the cell division protein DivIVA, correlating with altered cell morphology and peptidoglycan synthesis.
  • Daptomycin, DivIVA, and peptidoglycan reporters colocalize at membrane defect sites.

Conclusions:

  • Daptomycin primarily targets bacterial cell membranes, initiating a cascade of events.
  • This membrane disruption leads to the mislocalization of cell division and wall synthesis proteins, causing significant defects.
  • The study supports a mechanism involving primary membrane effects, ultimately leading to cell death.

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