ArticleMolecular biology of the cell2016
Abl suppresses cell extrusion and intercalation during epithelium folding.
Article in Molecular biology of the cell, 2016. 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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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
9 citing papers in PubMed.
- Inter-plane feedback coordinates cell morphogenesis and maintains 3D tissue organization in the Drosophila pupal retina.Development (Cambridge, England) · 2024Article
- Notch-dependent Abl signaling regulates cell motility during ommatidial rotation in Drosophila.Cell reports · 2022Article
- A modifier screen identifies regulators of cytoskeletal architecture as mediators of Shroom-dependent changes in tissue morphology.Biology open · 2021Article
- Abl and Canoe/Afadin mediate mechanotransduction at tricellular junctions.Science (New York, N.Y.) · 2020Article
- Orchestrating morphogenesis: building the body plan by cell shape changes and movements.Development (Cambridge, England) · 2020Review
- The Physical Mechanisms ofGenetics · 2020Article
- Mechanical impact of epithelial-mesenchymal transition on epithelial morphogenesis in Drosophila.Nature communications · 2019Article
- Tension, contraction and tissue morphogenesis.Development (Cambridge, England) · 2017Review
- Actomyosin-based tissue folding requires a multicellular myosin gradient.Development (Cambridge, England) · 2017Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Tissue morphogenesis requires control over cell shape changes and rearrangements. In the Drosophila mesoderm, linked epithelial cells apically constrict, without cell extrusion or intercalation, to fold the epithelium into a tube that will then undergo epithelial-to-mesenchymal transition (EMT). Apical constriction drives tissue folding or cell extrusion in different contexts, but the mechanisms that dictate the specific outcomes are poorly understood. Using live imaging, we found that Abelson (Abl) tyrosine kinase depletion causes apically constricting cells to undergo aberrant basal cell extrusion and cell intercalation. abl depletion disrupted apical-basal polarity and adherens junction organization in mesoderm cells, suggesting that extruding cells undergo premature EMT. The polarity loss was associated with abnormal basolateral contractile actomyosin and Enabled (Ena) accumulation. Depletion of the Abl effector Enabled (Ena) in abl-depleted embryos suppressed the abl phenotype, consistent with cell extrusion resulting from misregulated ena Our work provides new insight into how Abl loss and Ena misregulation promote cell extrusion and EMT.
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