ArticleCommunications biology2021
MAGIs regulate aPKC to enable balanced distribution of intercellular tension for epithelial sheet homeostasis.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- The temporal architecture of the seminiferous epithelial cycle revealed by spatial transcriptomics.Cell · 2026Article
- A steady-state pool of calcium-dependent actin is maintained by Homer and controls epithelial mechanosensation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cellular segregation in cocultures is driven by differential adhesion and contractility on distinct timescales.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- From lymphatic endothelial cell migration to formation of tubular lymphatic vascular network.Frontiers in physiology · 2023Review
- Apical-basal polarity and the control of epithelial form and function.Nature reviews. Molecular cell biology · 2022Review
- Tight Junction ZO Proteins Maintain Tissue Fluidity, Ensuring Efficient Collective Cell Migration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Synthetic dysmobility screen unveils an integrated STK40-YAP-MAPK system driving cell migration.Science advances · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Constriction of the apical plasma membrane is a hallmark of epithelial cells that underlies cell shape changes in tissue morphogenesis and maintenance of tissue integrity in homeostasis. Contractile force is exerted by a cortical actomyosin network that is anchored to the plasma membrane by the apical junctional complexes (AJC). In this study, we present evidence that MAGI proteins, structural components of AJC whose function remained unclear, regulate apical constriction of epithelial cells through the Par polarity proteins. We reveal that MAGIs are required to uniformly distribute Partitioning defective-3 (Par-3) at AJC of cells throughout the epithelial monolayer. MAGIs recruit ankyrin-repeat-, SH3-domain- and proline-rich-region-containing protein 2 (ASPP2) to AJC, which modulates Par-3-aPKC to antagonize ROCK-driven contractility. By coupling the adhesion machinery to the polarity proteins to regulate cellular contractility, we propose that MAGIs play essential and central roles in maintaining steady state intercellular tension throughout the epithelial cell sheet.
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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 OpenQuestion graph.