Hyperactivation of the Drosophila Hop Jak kinase causes the preferential overexpression of eIF1A transcripts in larval blood cells

Citation
Kv. Myrick et Cr. Dearolf, Hyperactivation of the Drosophila Hop Jak kinase causes the preferential overexpression of eIF1A transcripts in larval blood cells, GENE, 244(1-2), 2000, pp. 119-125
Citations number
39
Categorie Soggetti
Molecular Biology & Genetics
Journal title
GENE
ISSN journal
03781119 → ACNP
Volume
244
Issue
1-2
Year of publication
2000
Pages
119 - 125
Database
ISI
SICI code
0378-1119(20000222)244:1-2<119:HOTDHJ>2.0.ZU;2-L
Abstract
Jak kinase-Stat protein pathways play a critical role in the response of bl ood cells to a range of cytokines and growth factors. We are using the frui t fly, Drosophila melanogaster, as a model system to elucidate additional c omponents of Jak-Stat pathways, and to determine how abnormalities in this pathway lead to hematopoietic leukemia-like defects. To identify downstream targets, we conducted a molecular screen for genes whose transcripts are o verexpressed in response to activation of the Drosophila Hop Jak kinase. We identified a Drosophila homolog of eIF1A, a eukaryotic initiation factor f ound in humans and other eukaryotes. D-eIF1A is highly overexpressed in the hemocytes and lymph glands of third instar larvae carrying the dominant, g ain-of-function mutation hop(Tum-l). A quantitative comparison of poly(A)() RNA levels between D-eIF1A and other known Drosophila translation initiat ion factors indicates that D-eIF1A transcripts preferentially overaccumulat e in response to the hyperactive Hop pathway. Our results support the model that D-eIF1A is one of the target genes through which the Drosophila Jak k inase pathway regulates hemocyte development. (C) 2000 Elsevier Science B.V . All rights reserved.