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Citation
Maixner, A., Hecker, T.P., Phan, Q.N., 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(4): 347--361.
FlyBase ID
FBrf0105879
Publication Type
Research paper
Abstract
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.
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Dev. Genet.
    Title
    Developmental Genetics
    Publication Year
    1979-1999
    ISBN/ISSN
    0192-253X
    Data From Reference
    Aberrations (9)
    Alleles (85)
    Genes (60)
    Insertions (30)
    Transgenic Constructs (7)