Instant Membrane Stabilization by Damage-Triggered Actin Polymerization in Giant Unilamellar Vesicles

Area of Science:

• Biophysics
• Cell Biology
• Materials Science

Background:

• Giant unilamellar vesicles (GUVs) lack cellular repair mechanisms and rupture catastrophically when membrane pores enlarge.
• Understanding vesicle stabilization is crucial for artificial cell development and biomimetic studies.

Purpose of the Study:

• To develop a minimal, damage-triggered stabilization mechanism for GUVs.
• To investigate rapid actin polymerization as a method to prevent vesicle rupture.

Main Methods:

• Encapsulating ATP-activated G-actin in a divalent-cation-free lumen of GUVs.
• Exposing GUVs to external Ca²⁺ or Mg²⁺ to induce cation influx upon poration.
• Observing F-actin assembly and its effect on pore stabilization using microscopy.

Main Results:

• Localized cation entry upon membrane poration triggered rapid F-actin assembly.
• The assembled F-actin formed a cortical meshwork at the defect, arresting pore enlargement.
• Vesicle morphology was preserved for extended periods, demonstrating substantial survival against rupture.

Conclusions:

• A minimal, damage-triggered stabilization mechanism based on actin polymerization was successfully demonstrated in GUVs.
• This artificial system recapitulates the membrane wound response observed in single cells.
• The actin plug significantly enhances vesicle survival without fully restoring membrane impermeability.