Activation of a Drosophila Janus kinase (JAK) causes hematopoietic neoplasia and developmental defects.

  title={Activation of a Drosophila Janus kinase (JAK) causes hematopoietic neoplasia and developmental defects.},
  author={Douglas A. Harrison and Richard Binari and Theresa Stines Nahreini and Michael Gilman and Norbert Perrimon},
  journal={The EMBO Journal},
In mammals, many cytokines and growth factors stimulate members of the Janus kinase (JAK) family to transduce signals for the proliferation and differentiation of various cell types, particularly in hematopoietic lineages. Mutations in the Drosophila hopscotch (hop) gene, which encodes a JAK, also cause proliferative defects. Loss‐of‐function alleles result in lethality and underproliferation of diploid tissues of the larva. A dominant gain‐of‐function allele, Tumorous‐lethal (hopTum‐l), leads… 
A Genetic Screen Reveals an Unexpected Role for Yorkie Signaling in JAK/STAT-Dependent Hematopoietic Malignancies in Drosophila melanogaster
Results support a model in which elevated Yki signaling increases the number of hemocytes, which become melanotic tumors as a result of elevated JAK/STAT signaling.
Genetic Interactions between the Drosophila Tumor Suppressor Gene ept and the stat92E Transcription Factor
These findings identify ept as a cell-autonomous inhibitor of the Jak-Stat pathway and suggest that excess Jak-stat signaling makes a significant contribution to proliferative and tissue architectural phenotypes that occur in ept mutant tissues.
Mutation in the Jak kinase JH2 domain hyperactivates Drosophila and mammalian Jak-Stat pathways.
It is demonstrated that the mutant Hop proteins do indeed have increased tyrosine kinase activity, that the mutations hyperactivate the Hop-D-Stat pathway, and that Drosophila is a relevant system for the functional dissection of mammalian Jak-Stat pathways.
JAK signaling is somatically required for follicle cell differentiation in Drosophila.
Several roles for JAK signaling in Drosophila oogenesis are described, including a model in which Notch signaling determines a pool of cells to be competent to adopt stalk or polar fate, while Jak signaling assigns specific identity within that competent pool.
Pleiotropy of the Drosophila JAK pathway cytokine Unpaired 3 in development and aging.
Genomic organization of human JAK2 and mutation analysis of its JH2-domain in leukemia
A mutation analysis of the exons 13 to 19, encoding the kinase-like JH2 domain failed to detect activating mutations in leukemia samples, suggesting that this is a rare event in human leukemia.
A role for the Drosophila Toll/Cactus pathway in larval hematopoiesis.
The results suggest that the Toll/Cactus signal transduction pathway plays a significant role in regulating hemocyte proliferation and hemocyte density in the Drosophila larva.


The Genetics and Biology of Drosophila
This is the first attempt since 1925 to publish a comprehensive account of the biology and genetics of Drosophila and it aims to collate the dauntingly large literature on the subject and to make more accessible the private language ot the Dosophilist.
Molecular Cloning: A Laboratory Manual
The content has been entirely recast to include nucleic-acid based methods selected as the most widely used and valuable in molecular and cellular biology laboratories.
Antibodies: A
  • Hanratty,W.P. and Ryerse,J.S
  • 1981