ArticleMolecular biology of the cell2021
Myosin light chain kinase-driven myosin II turnover regulates actin cortex contractility during mitosis.
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 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Role of the nonhelical tailpiece of myosin-II in regulating filament architecture and function.The Journal of cell biology · 2026Article
- Review
- Dynamic insights into cellular mechanics and membrane undulations in vascular smooth muscle cells.American journal of physiology. Cell physiology · 2026Article
- Biophysical modeling identifies an optimal hybrid amoeboid-mesenchymal mechanism for maximal T cell migration speeds.Cell reports · 2026Article
- Aurora B maintains spherical shape of mitotic cells via simultaneously stabilizing myosin II and vimentin.Journal of molecular cell biology · 2025Article
- Biophysical modeling identifies an optimal hybrid amoeboid-mesenchymal mechanism for maximal T cell migration speeds.bioRxiv : the preprint server for biology · 2025Article
- A TLK2-mediated calcium-driven cell death pathway links neuronal degeneration to nuclear envelope disruption.Nature communications · 2025Article
- RhoA-ROCK2 signaling possesses complex pathophysiological functions in cancer progression and shows promising therapeutic potential.Cancer cell international · 2024Review
- Structure, regulation, and mechanisms of nonmuscle myosin-2.Cellular and molecular life sciences : CMLS · 2024Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Force generation by the molecular motor myosin II (MII) at the actin cortex is a universal feature of animal cells. Despite its central role in driving cell shape changes, the mechanisms underlying MII regulation at the actin cortex remain incompletely understood. Here we show that myosin light chain kinase (MLCK) promotes MII turnover at the mitotic cortex. Inhibition of MLCK resulted in an alteration of the relative levels of phosphorylated regulatory light chain (RLC), with MLCK preferentially creating a short-lived pRLC species and Rho-associated kinase (ROCK) preferentially creating a stable ppRLC species during metaphase. Slower turnover of MII and altered RLC homeostasis on MLCK inhibition correlated with increased cortex tension, driving increased membrane bleb initiation and growth, but reduced bleb retraction during mitosis. Taken together, we show that ROCK and MLCK play distinct roles at the actin cortex during mitosis; ROCK activity is required for recruitment of MII to the cortex, while MLCK activity promotes MII turnover. Our findings support the growing evidence that MII turnover is an essential dynamic process influencing the mechanical output of the actin cortex.
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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.