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Development. 2002 Sep;129(18):4241-8.

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

Author information

1
Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA. willis_li@URMC.Rochester.edu

Abstract

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.

PMID:
12183376
PMCID:
PMC3090254
[Indexed for MEDLINE]
Free PMC Article

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