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Patching plasma membrane disruptions with cytoplasmic membrane.

P L McNeil1, S S Vogel, K Miyake

  • 1Department of Cellular Biology and Anatomy, and Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, GA, USA. pmcneil@mail.mcg.edu.

Journal of Cell Science
|May 12, 2000
PubMed
Summary

Cell membrane repair uses a rapid fusion process. Reserve granules fuse to form a patch, sealing disruptions quickly and efficiently. This emergency mechanism differs from normal cell trafficking.

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Area of Science:

  • Cell Biology
  • Membrane Biology
  • Biophysics

Background:

  • Cellular membrane integrity is crucial for survival.
  • Plasma membrane disruptions can occur and require rapid repair.
  • Existing models of membrane resealing are insufficient to explain rapid repair.

Purpose of the Study:

  • To investigate the mechanism of rapid plasma membrane resealing.
  • To test the 'patch' hypothesis for membrane repair using sea urchin eggs.
  • To characterize the role of cytoplasmic organelles in membrane resealing.

Main Methods:

  • Studied sea urchin eggs undergoing plasma membrane disruption.
  • Monitored surface markers for plasma membrane proteins and lipids.
  • Assessed the dependence of resealing capacity on cytoplasmic organelles.

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  • Quantified the fusion kinetics and boundary formation of reserve granules.
  • Main Results:

    • Surface markers were initially absent at resealing sites, supporting the patch hypothesis.
    • Resealing capacity was dependent on the availability of fusion-competent reserve granules.
    • Reserve granules exhibited rapid, calcium-regulated fusion, forming large membrane boundaries.
    • Identified a distinct 'emergency' fusion mechanism for patch vesicle production.

    Conclusions:

    • Vesicle-vesicle fusion, particularly by reserve granules, provides a rapid mechanism for plasma membrane resealing.
    • This 'patch' mechanism is distinct from constitutive membrane trafficking pathways.
    • The findings reveal a novel cellular repair strategy essential for maintaining cell viability.