A gain-of-function mutation in Drosophila MAP kinase activates multiple receptor tyrosine kinase signaling pathways

Damian Brunner, Nadja Oellers, Janos Szabad, William H. Biggs, S. Lawrence Zipursky, Ernst Hafen

Research output: Contribution to journalArticle

367 Citations (Scopus)

Abstract

In the Drosophila eye, activation of the sevenless (sev) receptor tyrosine kinase is required for the specification of the R7 photoreceptor cell fate. In a genetic screen for mutations that result in the activation of the sev signaling pathway in the absence of the inducing signal, we identified a gain-of-function mutation in rolied (rlSevenmaker [rlSem]), which encodes a homolog of mitogen-activated protein (MAP) kinase. In addition to the sev pathway, this mutation activates the pathways controlled by torso and the epidermal growth factor receptor homolog. The rlSem mutation results in the substitution of a single conserved amino acid in the kinase domain. Activation of MAP kinase by the rlSem mutation is both necessary and sufficient to activate multiple signaling pathways controlled by receptor tyrosine kinases.

Original languageEnglish
Pages (from-to)875-888
Number of pages14
JournalCell
Volume76
Issue number5
DOIs
Publication statusPublished - Mar 11 1994

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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