Sluss H K, Davis R J
Program in Molecular Medicine, University of Massachusetts Medical School, Worcester 01605, USA.
J Cell Biochem. 1997 Oct 1;67(1):1-12.
The dorsal surface of the Drosophila embryo is formed by the migration of the lateral epithelial cells to cover the amnioserosa. The Drosophila cJun-N-terminal kinase (DJNK) is essential for this process. Mutations in DJNK or the DJNK activator hemipterous (HEP) lead to incomplete dorsal closure, resulting in a hole in the dorsal cuticle. The molecules downstream of DJNK in this signaling pathway have not been established. Here we demonstrate that the basket1 (bsk1) mutation of DJNK causes decreased interaction with DJUN. Expression of decapentaplegic (DPP), a TGF-beta homologue, in the leading edge of the dorsal epithelium, is identified as a genetic target of the JNK pathway. A constitutive allele of JUN is able to rescue the dorsal closure defect of bsk1 and restores DPP expression. Furthermore, ectopic DPP rescues the defects in dorsal closure caused by bsk1. These data indicate that the interaction of DJNK with DJUN contributes to the dorsal closure signaling pathway and targets DPP expression.
果蝇胚胎的背表面是由外侧上皮细胞迁移覆盖羊膜浆膜而形成的。果蝇cJun氨基末端激酶（DJNK）对于这一过程至关重要。DJNK或DJNK激活因子半翅目（HEP）的突变会导致背闭合不完全，从而在背角质层上形成一个洞。该信号通路中DJNK下游的分子尚未明确。在此我们证明，DJNK的basket1（bsk1）突变导致与DJUN的相互作用减少。TGF-β同源物——骨形态发生蛋白（DPP）在背上皮前缘的表达，被确定为JNK通路的一个遗传靶点。JUN的一个组成型等位基因能够挽救bsk1的背闭合缺陷并恢复DPP表达。此外，异位表达的DPP可挽救由bsk1引起的背闭合缺陷。这些数据表明，DJNK与DJUN的相互作用有助于背闭合信号通路并靶向DPP表达。
