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Identification of ras targets using a genetic approach
1Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley 94720.
Abstract:
The Sevenless receptor tyrosine kinase is required for the development of the R7 photoreceptor cell in the Drosophila eye. Several components of the Sevenless signal transduction pathway have been identified in genetic screens for enhancers/suppressors of the sevenless phenotype. These studies suggest that activation of Sevenless leads to stimulation of Ras1 activity, whereas Gap1 appears to act as a negative regulator of the pathway. Inactivation of the Gap1 locus causes transformation of non-neuronal cone cells into supernumerary R7 cells. This same mutant phenotype is observed when activated Ras1 is expressed under the control of the sevenless promoter. While studies in other organisms have demonstrated a role for ras gene products in signal transduction, the effectors of Ras activity have not yet been identified. We are carrying out genetic screens for enhancers and suppressors of the Gap1 and activated Ras1 phenotypes in the hope of identifying genes encoding some of these effectors. We are conducting chemical mutagenesis screens and have also screened existing collections of P element lines. A molecular characterization of the most promising mutations is in progress.
Insights
Researchers are identifying new genes that control cell development in Drosophila by studying the Sevenless signaling pathway. This research aims to uncover key effectors of Ras1 activity, crucial for understanding cell growth and differentiation.
Area of Science:
- Developmental Biology
- Molecular Biology
- Genetics
Background:
- The Sevenless receptor tyrosine kinase is essential for R7 photoreceptor cell development in Drosophila.
- Genetic screens have identified components of the Sevenless signal transduction pathway, including Ras1 activation and Gap1 negative regulation.
- Inactivating Gap1 or activating Ras1 under the Sevenless promoter causes non-neuronal cone cells to transform into supernumerary R7 cells.
Purpose of the Study:
- To identify novel genes encoding effectors of Ras1 activity.
- To further elucidate the Sevenless signal transduction pathway.
- To understand the genetic control of cell fate determination.
Main Methods:
- Genetic screens for enhancers and suppressors of Gap1 and activated Ras1 phenotypes.
- Chemical mutagenesis screens.
- Screening of existing P element insertion lines.
- Molecular characterization of identified mutations.
Main Results:
- Identification of mutations that modify the phenotypes associated with Gap1 inactivation and activated Ras1.
- Progress in the molecular characterization of promising mutations.
- Potential discovery of new genes involved in Ras1 signaling.
Conclusions:
- Genetic screens are effective in identifying components of developmental signaling pathways.
- The identified mutations are expected to reveal novel effectors of Ras1.
- This research contributes to understanding the molecular mechanisms of cell development and differentiation.