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doi:10.1534/genetics.105.046904
A more recent version of this article appeared on March 1, 2006.
REGULAR RESEARCH PAPERS |
Identification of Drosophila genes modulating JAK/STAT signal transduction
Tina Mukherjee 1, Ulrich Schaefer 1 and Martin P. Zeidler 1*
1 Max Planck Institute for Biophysical Chemistry
* To whom correspondence should be addressed. E-mail: mzeidle{at}gwdg.de.
Submitted on June 15, 2005
Revised on August 2, 2005
Accepted on 9 December 2005
The JAK/STAT pathway was first identified in mammals as a signaling mechanism central to hematopoiesis and has since been shown to exert a wide range of pleiotropic effects on multiple developmental processes. Its inappropriate activation is also implicated in the development of numerous human malignancies, especially those derived from hematopoietic lineages. The JAK/STAT signaling cascade has been conserved through evolution and although the pathway identified in Drosophila has been closely examined, the full complement of genes required to correctly transduce signaling in vivo remain to be identified. We have used a dosage sensitive dominant eye over-growth phenotype caused by ectopic activation of the JAK/STAT pathway to screen 2267 independent, newly generated mutagenic P-element insertions. After multiple rounds of retesting 23 interacting loci have been identified that represent genes not previously known to interact with JAK/STAT signaling. Analysis of these genes has identified three signal transduction pathways, seven potential components of the pathway itself and six putative downstream pathway target genes. The use of forward genetics to identify loci and reverse genetic approaches to characterize them has allowed us to assemble a collection of genes whose products represent novel components and regulators of this important signal transduction cascade.
Key Words:
Hopscotch, Janus Kinase, P{w+,GMR-
3'}, STAT92E, Unpaired
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