Differential requirement for STAT by gain-of-function and wild-type receptor tyrosine kinase Torso in Drosophila.

Published

Journal Article

Malignant transformation frequently involves aberrant signaling from receptor tyrosine kinases (RTKs). These receptors commonly activate Ras/Raf/MEK/MAPK signaling but when overactivated can also induce the JAK/STAT pathway, originally identified as the signaling cascade downstream of cytokine receptors. Inappropriate activation of STAT has been found in many human cancers. However, the contribution of the JAK/STAT pathway in RTK signaling remains unclear. We have investigated the requirement of the JAK/STAT pathway for signaling by wild-type and mutant forms of the RTK Torso (Tor) using a genetic approach in Drosophila. Our results indicate that the JAK/STAT pathway plays little or no role in signaling by wild-type Tor. In contrast, we find that STAT, encoded by marelle (mrl; DStat92E), is essential for the gain-of-function mutant Tor (Tor(GOF)) to activate ectopic gene expression. Our findings indicate that the Ras/Raf/MEK/MAPK signaling pathway is sufficient to mediate the normal functions of wild-type RTK, whereas the effects of gain-of-function mutant RTK additionally require STAT activation.

Full Text

Duke Authors

Cited Authors

  • Li, WX; Agaisse, H; Mathey-Prevot, B; Perrimon, N

Published Date

  • September 2002

Published In

Volume / Issue

  • 129 / 18

Start / End Page

  • 4241 - 4248

PubMed ID

  • 12183376

Pubmed Central ID

  • 12183376

International Standard Serial Number (ISSN)

  • 0950-1991

Language

  • eng

Conference Location

  • England