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Updated: Jun 18, 2026
09:54
Live-imaging of the Drosophila Pupal Eye
Published on: January 12, 2015
The dASPP-dRASSF8 complex regulates cell-cell adhesion during Drosophila retinal morphogenesis
Paul F Langton1, Julien Colombani, Eunice H Y Chan
1Apoptosis and Proliferation Control Laboratory, Cancer Research UK, London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.
Current Biology : CB
|November 26, 2009
Summary
Drosophila ASPP (dASPP) and RASSF8 proteins regulate adherens junctions (AJs) by controlling C-terminal Src kinase (dCsk) activity. This interaction fine-tunes cell adhesion during development and is conserved in humans.
Area of Science:
- Cell biology
- Developmental biology
- Molecular genetics
Background:
- Adherens junctions (AJs) are crucial for epithelial tissue structure and morphogenesis.
- AJs connect cells via E-cadherin and link to the actin cytoskeleton.
- Noncore AJ components modulate AJ plasticity during development.
Purpose of the Study:
- To investigate the role of dRASSF8 in conjunction with dASPP in regulating adherens junctions.
- To elucidate the molecular mechanism by which dASPP and dRASSF8 influence cell-cell adhesion and tissue development.
Main Methods:
- Genetic analysis in Drosophila.
- Biochemical interaction studies.
- Immunolocalization of proteins at adherens junctions.
Main Results:
- dRASSF8 binds to dASPP, stabilizing its levels and promoting dCsk activity.
- Both dASPP and dRASSF8 localize to AJs and are mutually required for localization.
- Loss of dRASSF8 or dASPP leads to abnormal E-cadherin localization and cellular arrangements.
Conclusions:
- dASPP and dRASSF8 fine-tune cell-cell adhesion by regulating dCsk and Src activity during Drosophila development.
- The dASPP-dRASSF8 interaction is conserved in humans, suggesting a role in restricting Src activity.
- Mammalian ASPP1/2 and RASSF8 may function as tumor suppressors by regulating Src proto-oncogene activity.
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