Membrane Tension and Cellular Dynamics

Cellular membranes are dynamic interfaces whose mechanical properties have emerged as central regulators of fundamental processes such as migration, morphogenesis and signal transduction. Membrane tension, defined as the in-plane force per unit length within the lipid bilayer, integrates cytoskeletal dynamics, trafficking and curvature-sensing machineries to shape cell behaviour. This tension is modulated by actin polymerisation, motor-driven contractility and membrane-to-cortex attachments, and influences processes ranging from protrusion formation to endocytic turnover. Recent work has revealed that membrane tension propagates across the cell surface on rapid timescales via flow of lipid–protein assemblies and that feedback between tension and biochemical pathways, such as phospholipase D2–mTORC2 signalling or caveolae-dependent mechanosensing, stabilises cell polarity and controls the spatiotemporal organisation of adhesion, endocytosis and migration in both two- and three-dimensional environments. These insights reshape our understanding of the plasma membrane as a load-bearing substrate that both responds to and directs the collective forces of the cytoskeleton, providing a unifying framework for cell shape regulation, tissue mechanics and pathological processes such as metastasis.

Research from Nature Portfolio

Experiments in epithelial cells have demonstrated that the ERM protein ezrin, which cross-links the actin cortex to the inner leaflet of the plasma membrane, is a key determinant of membrane tension and global cell stiffness. Manipulating ezrin activity alters tension measurements obtained by membrane tether extraction and leads to remodelling of cortical F-actin, highlighting its role as a molecular clutch governing cell mechanics. A complementary study has uncovered a dynamin-independent endocytic route, the CLIC/GEEC pathway, that is specifically upregulated upon decreases in membrane tension and in turn restores tension homeostasis. This mechanochemical feedback is mediated by the focal adhesion mechano-transducer vinculin, which controls levels of the ARF-GEF GBF1 at the surface. Finally, purely mechanical models of membrane remodelling have shown that cells accommodate shape changes through passive invaginations driven by local minimisation of bending and adhesion energies, which can be stored and released to buffer rapid area fluctuations before active remodelling occurs.

Membrane Tension and Cellular Dynamics publication trend

The graph below shows the total number of articles in membrane tension and cellular dynamics across all publications each year (not limited to Nature Index journals).

Technical terms

Membrane tension: The in-plane force per unit length within the lipid bilayer that resists membrane deformation.

Actin cortex: A thin network of cross-linked F-actin beneath the plasma membrane that provides structural support and transmits forces.

Mechanotransduction: The process by which cells convert mechanical stimuli into biochemical signals that regulate cellular functions.

CLIC/GEEC pathway: A dynamin-independent endocytic route that internalises GPI-anchored proteins and fluid-phase markers, contributing to membrane tension homeostasis.

BAR proteins: A family of curvature-sensing and curvature-generating proteins that regulate membrane shape and dynamics.

References

1. Ezrin is a Major Regulator of Membrane Tension in Epithelial Cells. Scientific Reports (2015).
2. Mechanochemical feedback control of dynamin independent endocytosis modulates membrane tension in adherent cells. Nature Communications (2018).
3. Physical principles of membrane remodelling during cell mechanoadaptation. Nature Communications (2015).
4. Cell protrusions and contractions generate long-range membrane tension propagation. Cell (2023).
5. Substrate Stiffness-Driven Membrane Tension Modulates Vesicular Trafficking via Caveolin‑1. ACS Nano (2022).
6. Membrane Tension Acts Through PLD2 and mTORC2 to Limit Actin Network Assembly During Neutrophil Migration. PLOS Biology (2016).