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
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.