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Published on: June 3, 2011
Akap200 suppresses the effects of Dv-cbl expression in the Drosophila eye
Rowena T Sannang1, Hannah Robertson, Nicole A Siddall
1Department of Anatomy and Neuroscience, University of Melbourne, Parkville, VIC, Australia.
Abstract:
The Drosophila melanogaster orthologue of the c-Cbl proto-oncogene acts to downregulate signalling from receptor tyrosine kinases by enhancing endocytosis of activated receptors. Expression of an analogue of the C-terminally truncated v-Cbl oncogene, Dv-cbl, in the developing Drosophila eye conversely leads to excess signalling and disruption to the well-ordered adult compound eye. Co-expression of activated Ras with Dv-cbl leads to a severe disruption of eye development. We have used a transposon-based inducible expression system to screen for molecules that can suppress the Dv-cbl phenotype and have identified an allele that upregulates the A-kinase anchoring protein, Akap200. Overexpression of Akap200 not only suppresses the phenotype caused by Dv-cbl expression, but also the severe disruption to eye development caused by the combined expression of Dv-cbl and activated Ras. Akap200 is also endogenously expressed in the developing Drosophila eye at a level that modulates the effects of excessive signalling caused by expression of Dv-cbl.
Insights
The A-kinase anchoring protein, Akap200, suppresses developmental eye defects in Drosophila caused by overactive signaling. This finding highlights Akap200's role in regulating receptor tyrosine kinase pathways.
Area of Science:
- Molecular Biology
- Developmental Biology
- Genetics
Background:
- The c-Cbl proto-oncogene regulates receptor tyrosine kinase (RTK) signaling by promoting receptor endocytosis.
- Aberrant RTK signaling contributes to developmental defects, as seen with the Drosophila v-Cbl oncogene analogue, Dv-cbl, in eye development.
Purpose of the Study:
- To identify suppressors of Dv-cbl-induced eye developmental defects using a Drosophila genetic screen.
- To investigate the role of identified suppressors in modulating RTK signaling pathways.
Main Methods:
- Utilized a transposon-based inducible expression system in Drosophila melanogaster.
- Conducted a genetic screen to identify mutations that suppress the Dv-cbl phenotype.
- Analyzed the effects of Akap200 overexpression on eye development in conjunction with Dv-cbl and activated Ras expression.
Main Results:
- Identified an Akap200 (A-kinase anchoring protein 200) allele that suppresses Dv-cbl-induced eye defects.
- Overexpression of Akap200 ameliorated phenotypes caused by both Dv-cbl alone and Dv-cbl plus activated Ras.
- Endogenous Akap200 expression levels in the developing eye modulate responses to excessive RTK signaling.
Conclusions:
- Akap200 acts as a suppressor of aberrant RTK signaling and associated developmental defects in Drosophila.
- Akap200 plays a crucial role in regulating signaling pathways that impact eye development.
