ArticleThe Journal of cell biology2011
Myosin IIA/IIB restrict adhesive and protrusive signaling to generate front-back polarity in migrating cells.
Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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Who cites it
94 citing papers in PubMed, 154 citations in OpenAlex.
- Paclitaxel induces NM2-dependent cellular contraction through GEF-H1 dissociation from microtubules and RhoA/ROCK activation in cancer cells.Molecular oncology · 2026Article
- MYH9 mutations differentially stabilize non-muscle myosin II filaments and induce distinct cellular aggregation phenotypes.Cellular and molecular life sciences : CMLS · 2026Article
- A song of heads and tails: myosin II conformational regulation and filament dynamics shape force generation in non-muscle cells.Biophysical reviews · 2026Review
- How Actin Polymerization and Myosin II Activity Regulate Focal Adhesion Dynamics in Motile Cells.International journal of molecular sciences · 2025Article
- Myosin II tension sensors visualize force generation within the actin cytoskeleton in living cells.Journal of cell science · 2024Article
- Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024Review
- Article
- Structure, regulation, and mechanisms of nonmuscle myosin-2.Cellular and molecular life sciences : CMLS · 2024Review
- Rho GTPase activity crosstalk mediated by Arhgef11 and Arhgef12 coordinates cell protrusion-retraction cycles.Nature communications · 2023Article
- MYH10 activation rescues contractile defects in arrhythmogenic cardiomyopathy (ACM).Nature communications · 2023Article
- Pulses of RhoA Signaling Stimulate Actin Polymerization and Flow in Protrusions to Drive Collective Cell Migration.bioRxiv : the preprint server for biology · 2023Article
- Migration and differentiation of muscle stem cells are coupled by RhoA signalling during regeneration.Open biology · 2023Article
- Persistent cell migration emerges from a coupling between protrusion dynamics and polarized trafficking.eLife · 2022Article
- Modeling cell protrusion predicts how myosin II and actin turnover affect adhesion-based signaling.Biophysical journal · 2022Article
- Article
- Microfluidic devices fitted with "flowver" paper pumps generate steady, tunable gradients for extended observation of chemotactic cell migration.Biomicrofluidics · 2021Article
- Myosin II and Arp2/3 cross-talk governs intracellular hydraulic pressure and lamellipodia formation.Molecular biology of the cell · 2021Article
- Targeting cytoskeletal phosphorylation in cancer.Exploration of targeted anti-tumor therapy · 2021Review
- Scribble, Lgl1, and myosin II form a complex in vivo to promote directed cell migration.Molecular biology of the cell · 2020Article
- Quantitative Phase Imaging of Spreading Fibroblasts Identifies the Role of Focal Adhesion Kinase in the Stabilization of the Cell Rear.Biomolecules · 2020Article
34 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Migratory front-back polarity emerges from the cooperative effect of myosin IIA (MIIA) and IIB (MIIB) on adhesive signaling. We demonstrate here that, during polarization, MIIA and MIIB coordinately promote localized actomyosin bundling, which generates large, stable adhesions that do not signal to Rac and thereby form the cell rear. MIIA formed dynamic actomyosin proto-bundles that mark the cell rear during spreading; it also bound to actin filament bundles associated with initial adhesion maturation in protrusions. Subsequent incorporation of MIIB stabilized the adhesions and actomyosin filaments with which it associated and formed a stable, extended rear. These adhesions did not turn over and no longer signal to Rac. Microtubules fine-tuned the polarity by positioning the front opposite the MIIA/MIIB-specified rear. Decreased Rac signaling in the vicinity of the MIIA/MIIB-stabilized proto-bundles and adhesions was accompanied by the loss of Rac guanine nucleotide exchange factor (GEFs), like βPIX and DOCK180, and by inhibited phosphorylation of key residues on adhesion proteins that recruit and activate Rac GEFs. These observations lead to a model for front-back polarity through local GEF depletion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.