ArticleiScience2023
Mechanosensitive accumulation of non-muscle myosin IIB during mitosis requires its translocation activity.
Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Yes-associated protein 1 in cancer: bridging mechanical transduction and epigenetic regulation.Cancer biology & therapy · 2025Review
- The mechanoresponsive chromosomal passenger complex sustains furrow ingression under confinement.Journal of molecular cell biology · 2025Article
- Nonmuscle myosin 2 turnover in cells is synergistically controlled by the tail and the motor domain.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Research progress on the regulatory role of cell membrane surface tension in cell behavior.Heliyon · 2024Review
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Authors and funding
6 authors.
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Abstract
Non-muscle myosin II (NMII) is a force-generating mechanosensitive enzyme that responds to mechanical forces. NMIIs mechanoaccumulate at the cell cortex in response to mechanical forces. It is essential for cells to mechanically adapt to the physical environment, failure of which results in mitotic defects when dividing in confined environment. Much less is known about how NMII mechanoaccumulation is regulated during mitosis. We show that mitotic cells respond to compressive stress by promoting accumulation of active RhoA at the cell cortex as in interphase cells. RhoA mechanoresponse during mitosis activates and stabilizes NMIIB via ROCK signaling, leading to NMIIB mechanoaccumulation at the cell cortex. Using disease-related myosin II mutations, we found that NMIIB mechanoaccumulation requires its motor activity that translocates actin filaments, but not just its actin-binding function. Thus, the motor activity coordinates structural movement and nucleotide state changes to fine-tune actin-binding affinity optimal for NMIIs to generate and respond to forces.
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