This article is a US Government work and, as such, is in the public domain in the United States of America.
A screen for mutations that prevent lethality caused by expression of activated sevenless and ras1 in the Drosophila embryo†
Article first published online: 31 DEC 1998
Copyright © 1998 Wiley-Liss, Inc.
Volume 23, Issue 4, pages 347–361, 1998
How to Cite
Maixner, A., Hecker, T. P., Phan, Q. N. and Wassarman, D. A. (1998), A screen for mutations that prevent lethality caused by expression of activated sevenless and ras1 in the Drosophila embryo. Dev. Genet., 23: 347–361. doi: 10.1002/(SICI)1520-6408(1998)23:4<347::AID-DVG9>3.0.CO;2-C
- Issue published online: 31 DEC 1998
- Article first published online: 31 DEC 1998
- Manuscript Accepted: 3 OCT 1998
- Manuscript Received: 14 AUG 1998
- Intramural Program in the National Institute of Child Health and Human Development
- Signal transduction;
- Trithorax group;
- eye development;
- receptor tyrosine kinase
Ras1 plays a critical role in receptor tyrosine kinase (RTK) signal transduction pathways that function during Drosophila development. We demonstrate that mis-expression of constitutively active forms of Ras1 (Ras1V12) and the Sevenless (Sev) RTK (SevS11) during embryogenesis causes lethality due to inappropriate activation of RTK/Ras1 signaling pathways. Genetic and molecular data indicate that the rate of SevS11/sev-Ras1V12 lethality is sensitive to the expression level of both transgenes. To identify genes that encode components of RTK/Ras1 signaling pathways or modulators of RNA polymerase II transcription, we took advantage of the dose-sensitivity of the system and screened for second site mutations that would dominantly suppress the lethality. The collection of identified suppressors includes the PR55 subunit of Protein Phosphatase 2A indicating that downstream of Sev and Ras1 this subunit acts as a negative regulator of phosphatase activity. The isolation of mutations in the histone deacetylase RPD3 suggests that it functions as positive regulator of sev enhancer-driven transcription. Finally, the isolation of mutations in the Trithorax group gene devenir and the characterized allelism with the Breathless RTK encoding gene provides evidence for Ras1-mediated regulation of homeotic genes. Dev. Genet. 23:347–361, 1998. © 1998 Wiley-Liss, Inc.