A SCREEN FOR MUTATIONS THAT PREVENT LETHALITY CAUSED BY EXPRESSION OF ACTIVATED SEVENLESS AND RAS1 IN THE DROSOPHILA EMBRYO

摘要: Ras1 plays a critical role in receptor tyrosine kinase (RTK) signal transduction pathways that function during Drosophila development. We demonstrate mis-expression of constitutively active forms (Ras1V12) and the Sevenless (Sev) RTK (SevS11) embryogenesis causes lethality due to inappropriate activation RTK/Ras1 signaling pathways. Genetic molecular data indicate rate SevS11/sev-Ras1V12 is sensitive expression level both transgenes. To identify genes encode components or modulators RNA polymerase II transcription, we took advantage dose-sensitivity system screened for second site mutations would dominantly suppress lethality. The collection identified suppressors includes PR55 subunit Protein Phosphatase 2A indicating downstream Sev this acts as negative regulator phosphatase activity. isolation histone deacetylase RPD3 suggests it functions positive sev enhancer-driven transcription. Finally, Trithorax group gene devenir characterized allelism with Breathless encoding provides evidence Ras1-mediated regulation homeotic genes. Dev. Genet. 23:347–361, 1998. © 1998 Wiley-Liss, Inc.