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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 ( N CK- i nteracting k inase [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.

genes and development

The <i>Drosophila</i> Ste20-related kinase <i>misshapen </i>is required for embryonic dorsal closure and acts through a JNK MAPK module on an evolutionarily conserved signaling pathway

The Drosophila Ste20-related kinase misshapen is required for embryonic dorsal closure and acts through a JNK MAPK module on an evolutionarily conserved signaling pathway