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Vol. 12, No. 15, pp. 2371-2380, August 1, 1998
1 Department of Pharmacology and
2 Department of
Cell Biology, New York University Medical Center, Skirball Institute
of Biomolecular Medicine, New York, New York 10016 USA
Dorsal closure in the Drosophila embryo occurs during the
later stages of embryogenesis and involves changes in cell shape leading to the juxtaposition and subsequent adherence of the lateral epidermal primordia over the amnioserosa. Dorsal closure requires the
activation of a conserved c-jun amino-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) module, as it is blocked by
null mutations in JNK kinase [hemipterous (hep)] and JNK
[basket (bsk)]. Drosophila JNK (DJNK) functions by
phosphorylating and activating DJun, which in turn induces the
transcription of decapentaplegic (dpp). We provide
biochemical and genetic evidence that a Ste20-related kinase,
misshapen (msn), functions upstream of hep and
bsk to stimulate dorsal closure in the Drosophila
embryo. Mammalian (NCK-interacting kinase [NIK]) and Caenorhabditis elegans
(mig-15) homologs of msn have been identified;
mig-15 is necessary for several developmental processes in
C. elegans. These data suggest that msn, mig-15, and
NIK are components of a signaling pathway that is conserved among
flies, worms, and mammals to control developmentally regulated pathways.
[Key Words: Drosophila; Ste20 kinase; NIK; misshapen; dorsal closure; JNK]
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