ArticleProceedings of the National Academy of Sciences of the United States of America2020
Actin protrusions push at apical junctions to maintain E-cadherin adhesion.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
43 citing papers in PubMed, 89 citations in OpenAlex.
- Bulk delivery of a preassembled apical surface initiates epithelial lumen formation.Nature communications · 2026Article
- Moderately Reduced Contractility Decreases Epithelial Cell-Cell Contact Rupture Under Large External Stretch.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms of active wetting and fluidification in epithelial cell collectives.Nature materials · 2026Article
- Cell loss disrupts mechanical homeostasis to drive retinal pigment epithelium ageing-like phenotype in vitro.Nature communications · 2026Article
- Actomyosin-dependent assembly of the mechanosensitive machinery from adherens junctions triggers actin polymerization and organization.Science advances · 2026Article
- AI driven 3D subcellular RPE map discovers cell state transitions in establishment of apical-basal polarity.NPJ artificial intelligence · 2026Article
- Hirudin suppresses hematogenous metastasis by targeting desmosome junction transition in circulating tumor cell clusters via HIF-1α-DSG2 signaling.Experimental & molecular medicine · 2025Article
- Cadherin dynamics and cortical tension in remodeling cell-cell adhesion during EMT.Biophysical journal · 2025Article
- Cell signaling facilitates apical constriction by basolaterally recruiting Arp2/3 via Rac and WAVE.The Journal of cell biology · 2025Article
- Article
- Vinculin-Arp2/3 interaction inhibits branched actin assembly to control migration and proliferation.Life science alliance · 2025Article
- NHSL3 controls single and collective cell migration through two distinct mechanisms.Nature communications · 2025Article
- Model supports asymmetric regulation across the intercellular junction for collective cell polarization.PLoS computational biology · 2024Article
- Actin-templated Structures: Nature's Way to Hierarchical Surface Patterns (Gecko's Setae as Case Study).Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Advances in modeling cellular mechanical perceptions and responses via the membrane-cytoskeleton-nucleus machinery.Mechanobiology in medicine · 2024Review
- Changes of Ex Vivo Cervical Epithelial Cells Due to Electroporation with JMY.International journal of molecular sciences · 2023Article
- Dynamics and functions of E-cadherin complexes in epithelial cell and tissue morphogenesis.Marine life science & technology · 2023Review
- MAP4K4 regulates forces at cell-cell and cell-matrix adhesions to promote collective cell migration.Life science alliance · 2023Article
- Engineering tools for quantifying and manipulating forces in epithelia.Biophysics reviews · 2023Review
- APC-driven actin nucleation powers collective cell dynamics in colorectal cancer cells.iScience · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cadherin-mediated cell-cell adhesion is actin-dependent, but the precise role of actin in maintaining cell-cell adhesion is not fully understood. Actin polymerization-dependent protrusive activity is required to push distally separated cells close enough to initiate contact. Whether protrusive activity is required to maintain adhesion in confluent sheets of epithelial cells is not known. By electron microscopy as well as live cell imaging, we have identified a population of protruding actin microspikes that operate continuously near apical junctions of polarized Madin-Darby canine kidney (MDCK) cells. Live imaging shows that microspikes containing E-cadherin extend into gaps between E-cadherin clusters on neighboring cells, while reformation of cadherin clusters across the cell-cell boundary correlates with microspike withdrawal. We identify Arp2/3, EVL, and CRMP-1 as 3 actin assembly factors necessary for microspike formation. Depleting these factors from cells using RNA interference (RNAi) results in myosin II-dependent unzipping of cadherin adhesive bonds. Therefore, actin polymerization-dependent protrusive activity operates continuously at cadherin cell-cell junctions to keep them shut and to prevent myosin II-dependent contractility from tearing cadherin adhesive contacts apart.
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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.