ArticleNature communications2025
A feedback circuitry involving γ-actin, β-actin and nonmuscle myosin-2 A controls tight junction and apical cortex mechanics.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Single-cell transcriptomics and multimodal molecular profiling revealed the oncogenesis and tumor microenvironment of cardiac myxoma.Science China. Life sciences · 2026Article
- Deep learning-supported image quantification of epithelial cell shapes and its application to polycystic kidney disease.PLoS computational biology · 2026Article
- Single Cell Mechanics in Disease Progression.Small science · 2026Review
- Mechanics of blunting of actin-myosin interaction dynamics by the actinopathy-causing mutation E334Q in cytoskeletal γ-actin.The Journal of physiology · 2026Article
- Article
- A feedback circuitry involving γ-actin, β-actin and nonmuscle myosin-2 A controls tight junction and apical cortex mechanics.Nature communications · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
Cytoplasmic β- and γ-actin isoforms, along with non-muscle myosin 2 isoforms, are tightly regulated in epithelial cells and compose the actomyosin cytoskeleton at the apical junctional complex. However, their specific role in regulating the mechanics of the membrane cortex and the organization of junctions, and which biomechanical circuitries modulate their expression remain poorly understood. Here, we show that γ-actin depletion in MDCK and other epithelial cells results in increased expression and junctional accumulation of β-actin and increased tight junction membrane tortuosity, both dependent on nonmuscle myosin-2A upregulation. The knock-out of γ-actin also decreases apical membrane stiffness and increases dynamic exchange of the cytoplasmic tight junction proteins like ZO-1 and cingulin, without affecting tight junction organization and barrier function. In summary, our findings uncover a biomechanical circuitry linking γ-actin to β-actin expression through nonmuscle myosin-2A and reveal γ-actin as a key regulator of tight junction and apical membrane cortex mechanics, and the dynamics of cytoskeleton-associated tight junction proteins in epithelial cells.
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Registered trials
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