ArticleMolecular biology of the cell2023
Coordinated efforts of different actin filament populations are needed for optimal cell wound repair.
Article in Molecular biology of the cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Curving Actin Across Systems: Do Axonal Actin Rings Share Common Underlying Mechanisms?Journal of neurochemistry · 2026Review
- Toggle-Untoggle - a cell segmentation tool with an interactive user verification interface.Journal of cell science · 2025Article
- Reactive oxygen species counteract zebrafish wound contraction and promote wound healing.Biophysical journal · 2025Article
- Overexpression of Drosophila NUAK or Constitutively-Active Formin-Like Promotes the Formation of Aberrant Myofibrils.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Septin complexes: Ahead of the curve.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Calcium influx rapidly establishes distinct spatial recruitments of Annexins to cell wounds.Genetics · 2024Article
- Two Septin complexes mediate actin dynamics during cell wound repair.Cell reports · 2024Article
- Tumor invasiveness is regulated by the concerted function of APC, formins, and Arp2/3 complex.iScience · 2024Article
- Patterning of the cell cortex by Rho GTPases.Nature reviews. Molecular cell biology · 2024Review
- Wound Repair of the Cell Membrane: Lessons fromCells · 2024Review
- Two Septin Complexes Mediate Actin Dynamics During Cell Wound Repair.bioRxiv : the preprint server for biology · 2023Article
- Scar/WAVE has Rac GTPase-independent functions during cell wound repair.Scientific reports · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cells are subjected to a barrage of daily insults that often lead to their cortices being ripped open and requiring immediate repair. An important component of the cell's repair response is the formation of an actomyosin ring at the wound periphery to mediate its closure. Here we show that inhibition of myosin or the linear actin nucleation factors Diaphanous and/or dishevelled associated activator of morphogenesis results in a disrupted contractile apparatus and delayed wound closure. We also show that the branched actin nucleators WASp and SCAR function nonredundantly as scaffolds to assemble and maintain this contractile actomyosin cable. Removing branched actin leads to the formation of smaller circular actin-myosin structures at the cell cortex and to slow wound closure. Removing linear and branched actin simultaneously results in failed wound closure. Surprisingly, removal of branched actin and myosin results in the formation of parallel linear F-actin filaments that undergo a chiral swirling movement to close the wound, uncovering a new mechanism of cell wound closure. Taken together, we demonstrate the roles of different actin substructures that are required for optimal actomyosin ring formation and the extraordinary resilience of the cell to undergo wound repair when it is unable to form different subsets of these substructures.
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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 Socratic graph.