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Published on: December 16, 2009
A screen for genes that function downstream of Ras1 during Drosophila eye development
F D Karim1, H C Chang, M Therrien
1Howard Hughes Medical Institute, University of California, Berkeley 94720-3200, USA.
Abstract:
Cell-fate specification of the R7 photoreceptor cell is controlled by the sevenless receptor tyrosine kinase (SevRTK) and Ras1, the Drosophila homologue of mammalian H-ras, K-ras and N-ras oncogenes. An activated form of Ras1 expressed under control of the sevenless enhancer/promoter (sev-Ras1V12) induces production of supernumerary R7 photoreceptor cells, which causes the eye to become rough in appearance. To isolate mutations in genes functioning downstream of Ras1, we carried out a screen for dominant suppressors and enhancers of this rough eye phenotype. Approximately 850,000 mutagenized flies were screened, and 282 dominant suppressors and 577 dominant enhancers were isolated. Mutations in the Drosophila homologues of Raf, MEK, MAPK, type I Geranylgeranyl Transferase and Protein Phosphatase 2A were isolated, as were mutations in several novel signaling genes. Some of these mutant genes appear to be general signaling factors that function in other Ras1 pathways, while one seems to be more specific for photoreceptor development. At least two suppressors appear to function either between Ras1 and Raf or in parallel to Raf.
Insights
Researchers screened over 850,000 flies to identify genes downstream of Ras1 signaling in Drosophila eye development. They discovered novel genes and known pathway components, including Raf and MEK, that regulate cell-fate specification.
Area of Science:
- Developmental Biology
- Cell Signaling
- Genetics
Background:
- Cell-fate specification in Drosophila R7 photoreceptor cells is regulated by the sevenless receptor tyrosine kinase (SevRTK) and Ras1 signaling pathway.
- Overexpression of activated Ras1 (sev-Ras1V12) leads to supernumerary R7 cells and a rough eye phenotype, providing a basis for genetic screens.
Purpose of the Study:
- To identify genes functioning downstream of Ras1 in the sevenless pathway.
- To isolate dominant suppressors and enhancers of the sev-Ras1V12-induced rough eye phenotype.
Main Methods:
- A large-scale genetic screen of approximately 850,000 mutagenized Drosophila was conducted.
- Dominant suppressors and enhancers of the rough eye phenotype caused by sev-Ras1V12 were isolated and characterized.
Main Results:
- 282 dominant suppressors and 577 dominant enhancers were identified.
- Mutations were found in Drosophila homologues of Raf, MEK, MAPK, Geranylgeranyl Transferase, and Protein Phosphatase 2A.
- Novel signaling genes were discovered, some acting as general Ras1 pathway components and others specific to photoreceptor development.
Conclusions:
- The screen successfully identified key components of the Ras1 signaling pathway involved in R7 photoreceptor cell-fate specification.
- At least two suppressors suggest novel interactions, potentially acting between Ras1 and Raf or in parallel to Raf.
- This study provides insights into the complex genetic network regulating photoreceptor development in Drosophila.
