ArticleThe Journal of cell biology2025
α-Catenin force-sensitive binding and sequestration of LZTS2 leads to cytokinesis failure.
Article in The Journal of cell biology, 2025. 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.
- A screen for adherens junction proteins regulating collective cell migration and testis morphogenesis reveals important roles for the Rab GAP RN-tre and the kinase Par-1.Molecular biology of the cell · 2026Article
- A screen for adherens junction proteins regulating collective cell migration and testis morphogenesis reveals important roles for the Rab GAP RN-tre and the kinase Par-1.bioRxiv : the preprint server for biology · 2026Article
- Intact Mass Profiling Reveals Phospho-Proteoforms of the Catenins (85-110 kDa) Regulated by Actomyosin Contractility.Angewandte Chemie (International ed. in English) · 2025Article
- α-catenin phosphorylation is actomyosin-sensitive and required for epithelial barrier functions through Afadin.bioRxiv : the preprint server for biology · 2025Article
- Neighbor cells restrain furrowing during Xenopus epithelial cytokinesis.Developmental cell · 2025Article
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12 authors.
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Abstract
Epithelial cells can become polyploid upon tissue injury, but mechanosensitive cues that trigger this state are poorly understood. Using an Madin Darby Canine Kidney (MDCK) cell knock-out/reconstitution system, we show that α-catenin mutants that alter force-sensitive binding to F-actin or middle (M)-domain promote cytokinesis failure and binucleation, particularly near epithelial wound-fronts. We identified Leucine Zipper Tumor Suppressor 2 (LZTS2), a factor previously implicated in abscission, as a conformation sensitive proximity partner of α-catenin. We show that LZTS2 enriches not only at midbody/intercellular bridges but also at apical adhering junctions. α-Catenin mutants with persistent M-domain opening show elevated junctional enrichment of LZTS2 compared with wild-type cells. LZTS2 knock-down leads to elevated rates of binucleation. These data implicate LZTS2 as a mechanosensitive effector of α-catenin that is critical for cytokinetic fidelity. This model rationalizes how persistent mechanoactivation of α-catenin may drive tension-induced polyploidization of epithelia after injury and suggests an underlying mechanism for how pathogenic α-catenin M-domain mutations drive macular dystrophy.
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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 Socratic graph.