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Background <p>Robust coordination of surface and volume changes is critical for cell integrity. Few studies have elucidated the plasma membrane (PM) remodeling events during drastic cell surface and volume alteration, especially regarding PM sensing and its subsequent rearrangements.</p> Results <p>In this article, using fission yeast protoplasts, we reveal a Ca<sup>2+</sup>-dependent mechanism for membrane addition that ensures PM integrity and allows its expansion during acute hypoosmotic cell swelling. We show that MscS-like mechanosensitive channels activated by PM tension control extracellular Ca<sup>2+</sup> influx, which triggers potential direct lipid transfer at endoplasmic reticulum (ER)-PM contact sites by conserved extended-synaptotagmins and accelerates exocytosis, enabling PM expansion necessary for osmotic equilibrium. Defects in any of these key events result in rapid protoplast rupture upon severe hypotonic shock. Our numerical simulations of such hypoosmotic PM expansion further propose a cellular strategy that combines instantaneous non-vesicular lipid transfer with bulk exocytic membrane delivery to maintain PM integrity for dramatic cell surface/volume adaptation.</p> Conclusions <p>We propose a cellular strategy that combines instantaneous non-vesicular lipid transfer with bulk exocytic membrane delivery to maintain PM integrity for dramatic cell surface/volume adaptation.</p>

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Ca2+-dependent vesicular and non-vesicular lipid transfer controls hypoosmotic plasma membrane expansion

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月9日

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  • Baicong Mu,
  • David M. Rutkowski,
  • Gianluca Grenci,
  • Dimitrios Vavylonis,
  • Dan Zhang

摘要

Background

Robust coordination of surface and volume changes is critical for cell integrity. Few studies have elucidated the plasma membrane (PM) remodeling events during drastic cell surface and volume alteration, especially regarding PM sensing and its subsequent rearrangements.

Results

In this article, using fission yeast protoplasts, we reveal a Ca2+-dependent mechanism for membrane addition that ensures PM integrity and allows its expansion during acute hypoosmotic cell swelling. We show that MscS-like mechanosensitive channels activated by PM tension control extracellular Ca2+ influx, which triggers potential direct lipid transfer at endoplasmic reticulum (ER)-PM contact sites by conserved extended-synaptotagmins and accelerates exocytosis, enabling PM expansion necessary for osmotic equilibrium. Defects in any of these key events result in rapid protoplast rupture upon severe hypotonic shock. Our numerical simulations of such hypoosmotic PM expansion further propose a cellular strategy that combines instantaneous non-vesicular lipid transfer with bulk exocytic membrane delivery to maintain PM integrity for dramatic cell surface/volume adaptation.

Conclusions

We propose a cellular strategy that combines instantaneous non-vesicular lipid transfer with bulk exocytic membrane delivery to maintain PM integrity for dramatic cell surface/volume adaptation.