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Abl suppresses cell extrusion and intercalation during epithelium folding
Jeanne N Jodoin1, Adam C Martin2
1Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142.
Molecular Biology of the Cell
|July 22, 2016
Summary
Abelson (Abl) tyrosine kinase depletion in Drosophila mesoderm causes cell extrusion and premature epithelial-mesenchymal transition (EMT). Misregulated Enabled (Ena) is key to this process, impacting cell polarity and tissue morphogenesis.
Area of Science:
- Developmental Biology
- Cell Biology
- Molecular Biology
Background:
- Tissue morphogenesis relies on precise cell shape changes and rearrangements.
- Apical constriction is a key mechanism in epithelial tube formation and cell extrusion.
- The factors dictating outcomes of apical constriction remain incompletely understood.
Purpose of the Study:
- To investigate the role of Abelson (Abl) tyrosine kinase in Drosophila mesoderm morphogenesis.
- To elucidate the mechanisms by which Abl influences cell shape, polarity, and epithelial-mesenchymal transition (EMT).
- To identify downstream effectors of Abl involved in regulating cell extrusion.
Main Methods:
- Live imaging of Drosophila embryos.
- Genetic depletion of Abelson (Abl) tyrosine kinase.
- Analysis of apical-basal polarity and adherens junction organization.
- Investigation of actomyosin dynamics and Enabled (Ena) protein localization.
Main Results:
- Abl depletion induced aberrant basal cell extrusion and intercalation in the mesoderm.
- Loss of Abl disrupted apical-basal polarity and adherens junctions.
- Abnormal basolateral actomyosin and Ena accumulation were observed in abl-depleted cells.
- Depletion of Ena suppressed the extrusion phenotype in abl-depleted embryos.
Conclusions:
- Abl kinase activity is crucial for maintaining cell polarity and preventing aberrant cell extrusion during Drosophila mesoderm development.
- Misregulation of the Abl effector Enabled (Ena) contributes to cell extrusion and premature EMT.
- This study provides novel insights into the molecular control of cell extrusion and EMT by Abl and Ena.
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