ArticleMolecular biology of the cell2021
Myosin II and Arp2/3 cross-talk governs intracellular hydraulic pressure and lamellipodia formation.
Article in Molecular biology of the cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 16 citations in OpenAlex.
- CFM: confinement force microscopy-a dynamic, precise and stable microconfiner for traction force microscopy in spatial confinement.Nature methods · 2026Article
- Hydrostatic pressure reduces the mechanosensitivity of cell migration.Science advances · 2026Article
- Osmotic Tension Asymmetry Drives Electrotactic Migration via PDLIM7-Polarized Microfilament Coordination in Breast Cancer Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Biophysical modeling identifies an optimal hybrid amoeboid-mesenchymal mechanism for maximal T cell migration speeds.Cell reports · 2026Article
- Decoding Rho GTPase signalling networks in directed cell migration.Frontiers in cell and developmental biology · 2026Review
- Coordinated Arp2/3-mediated actin branching and myosin-dependent force generation in membrane-cytoskeleton remodeling.Frontiers in physiology · 2026Review
- Emerging role of long non‑coding RNAs in the Rho/ROCK signaling pathway in tumor metastasis (Review).International journal of molecular medicine · 2025Review
- FGD3 mediates lytic cell death, enhancing efficacy and immunogenicity of chemotherapy agents in breast cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Biophysical modeling identifies an optimal hybrid amoeboid-mesenchymal mechanism for maximal T cell migration speeds.bioRxiv : the preprint server for biology · 2025Article
- GαInternational journal of molecular sciences · 2025Article
- AKBA Promotes Axonal Regeneration via RhoA/Rictor to Repair Damaged Sciatic Nerve.International journal of molecular sciences · 2022Article
- Cell-3D matrix interactions: recent advances and opportunities.Trends in cell biology · 2022Review
- Article
- miR-195 regulates intestinal epithelial restitution after wounding by altering actin-related protein-2 translation.American journal of physiology. Cell physiology · 2022Article
- Non-muscle myosin II and the plasticity of 3D cell migration.Frontiers in cell and developmental biology · 2022Review
- Cytoplasmic pressure maintains epithelial integrity and inhibits cell motility.Physical biology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Human fibroblasts can switch between lamellipodia-dependent and -independent migration mechanisms on two-dimensional surfaces and in three-dimensional (3D) matrices. RhoA GTPase activity governs the switch from low-pressure lamellipodia to high-pressure lobopodia in response to the physical structure of the 3D matrix. Inhibiting actomyosin contractility in these cells reduces intracellular pressure and reverts lobopodia to lamellipodial protrusions via an unknown mechanism. To test the hypothesis that high pressure physically prevents lamellipodia formation, we manipulated pressure by activating RhoA or changing the osmolarity of the extracellular environment and imaged cell protrusions. We find RhoA activity inhibits Rac1-mediated lamellipodia formation through two distinct pathways. First, RhoA boosts intracellular pressure by increasing actomyosin contractility and water influx but acts upstream of Rac1 to inhibit lamellipodia formation. Increasing osmotic pressure revealed a second RhoA pathway, which acts through nonmuscle myosin II (NMII) to disrupt lamellipodia downstream from Rac1 and elevate pressure. Interestingly, Arp2/3 inhibition triggered a NMII-dependent increase in intracellular pressure, along with lamellipodia disruption. Together, these results suggest that actomyosin contractility and water influx are coordinated to increase intracellular pressure, and RhoA signaling can inhibit lamellipodia formation via two distinct pathways in high-pressure cells.
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