# Dynamic mechanisms for membrane skeleton transitions

**Authors:** Mayte Bonilla-Quintana, Andrea Ghisleni, Nils C. Gauthier, Padmini Rangamani

PMC · DOI: 10.1242/jcs.263473 · 2025-02-28

## TL;DR

This paper explores how the cell's membrane skeleton, especially spectrin and myosin, dynamically responds to mechanical stress and maintains cell structure.

## Contribution

A new generalized network model was developed to study membrane skeleton transitions under mechanical stress.

## Key findings

- Membrane bending forces are crucial for maintaining a regular skeletal structure.
- Spectrin and myosin turnover is necessary for transitions between stress and rest states.
- Cell attachment through adhesions stabilizes cell shape.

## Abstract

The plasma membrane and the underlying skeleton form a protective barrier for eukaryotic cells. The molecular players forming this complex composite material constantly rearrange under mechanical stress. One of those molecules, spectrin, is ubiquitous in the membrane skeleton and linked by short actin filaments. In this work, we developed a generalized network model for the membrane skeleton integrating myosin contractility and membrane mechanics to investigate the response of the spectrin meshwork to mechanical loading. We observed that the force generated by membrane bending is important in maintaining a regular skeletal structure, suggesting that the membrane is not just supported by the skeleton, but actively contributes towards the stability of the cell structure. We found that spectrin and myosin turnover are necessary for the transition between stress and rest states in the skeleton. Simulations of a fully connected network representing a whole cell show that the surface area constraint of the plasma membrane and volume restriction of the cytoplasm enhance the stability of the membrane skeleton. Furthermore, we showed that cell attachment through adhesions promotes cell shape stabilization.

Summary: A model of the spectrin skeleton reveals mechanisms that are necessary to respond to external stresses. Moreover, it shows how global signals support skeletal structure and enhance its stability.

## Linked entities

- **Proteins:** beta-Spec (beta Spectrin), MYH14 (myosin heavy chain 14)

## Full-text entities

- **Genes:** MYH14 (myosin heavy chain 14) [NCBI Gene 79784] {aka DFNA4, DFNA4A, FP17425, MHC16, MYH17, NMHC II-C}

## Figures

50 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11928055/full.md

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Source: https://tomesphere.com/paper/PMC11928055