Abl suppresses cell extrusion and intercalation during epithelium folding
Name
Jodoin-2016-Abl suppresses cell.pdf
Size
11.12 MB
Format
Adobe PDF
Checksum (MD5)
1de4999169c897cacb7dba3ed428a517
Author(s)
Jodoin, Jeanne
Martin, Adam C
Date Issued
July 2016
Journal
Molecular Biology of the Cell
Publisher
American Society for Cell Biology
Citation
Jodoin, J. N., and A. C. Martin. “Abl Suppresses Cell Extrusion and Intercalation during Epithelium Folding.” Molecular Biology of the Cell 27.18 (2016): 2822–2832.
Version
Final published version
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.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Terms of Use
Creative Commons Attribution-NonCommercial-ShareAlike 3.0
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DOI of Published Version
https://doi.org/10.1091/mbc.E16-05-0336
