Drosophila Jun kinase regulates expression of decapentaplegic via the ETS-domain protein Aop and the AP-1 transcription factor DJun during dorsal closure.

Stress signaling in Drosophila

“…Lateral cells never elongate when the JNK signaling cascade is blocked by mutation suggesting that Dpp, a JNK pathway transcriptional target and secreted factor, may mediate the ventrally directed wave of cellular elongation observed in wildtype embryos during DC. LE expression of a constitutively activated form of c-Jun, Jun act , is capable of rescuing not only the cuticle phenotype caused by mutations in either bsk or hep but also of restoring dpp expression at the LE and cell elongation in the lateral epidermis (Hou et al, 1997; Riesgo-Escovar and Hafen, 1997). These results emphasize several important facets of the JNK signaling cascade and the DC system in general.…”

“…Loss of JNK pathway activity has (Glise & Noselli, 1997;Harden et al, 1995;1999) (Glise & Noselli, 1997;Harden et al, 1995;1999 (Padgett et al, 1987;Gelbart, 1987) (A olter et al, 1994;Brummel et al, 1994;Nellen et al, 1994;Penton et al, 1994) Ruberte et al, 1995) (Hudson et al, 1998) (Das et al, 1998;Hudson et al, 1998;Wisotzkey et al, 1998) Grieder et al, 1995;Staehling-Hampton et al, 1995) several consequences that contribute to a failure of DC. Mutant embryos exhibit a loss of dpp expression in LE cells without perturbing other elements of the dpp expression pattern (Glise and Noselli, 1997;Hou et al, 1997;Riesgo-Escovar and Hafen, 1997). puc expression is similarly a ected.…”

“…A prediction of this model linking the two signaling pathways is that restoration of Dpp signaling should alleviate the block to DC caused by mutations in positively acting components of the JNK pathway. Indeed, targeted expression in lateral epidermal cells of an activated Dpp receptor, tkv act , rescues partially the loss of bsk or DJun function presumably by mediating the e ects of Dpp in the lateral cells (Hou et al, 1997;Riesgo-Escovar and Hafen, 1997). Taken together with biochemical experiments demonstrating the catalytic activity and substrate speci®city of Hep (JNKK) and Bsk (JNK) Sluss et al, 1996), these results con®rm that the components of the JNK signaling cascade in Drosophila functionally resemble the stress signaling kinase cascades de®ned in yeast and vertebrates.…”

Diverse functions of JNK signaling and c-Jun in stress response and apoptosis

“…In Drosophila, evidence has been presented for an involvement of Jun in several developmental processes. It has been shown that Drosophila Jun can induce photoreceptor di erentiation after being phosphorylated by Drosophila ERK (Bohmann et al, 1994;Peverali et al, 1996) and that it acts as an e ector of JNK signaling in the regulation of morphogenetic cellCellular responses to c-Jun and JNK signaling S Leppa È and D Bohmann shape changes (Kockel et al, 1997;Riesgo-Escovar and Hafen, 1997). …”

The use of whole‐mount in situ hybridization to illustrate gene expression regulation

“…The JNK pathway is required during DC for the elongation of the lateral epidermis and to regulate the formation of a contractile actomyosin cable. It also controls the expression of the decapentaplegic (dpp) and puckered (puc) genes in the dorsal-most epidermal (DME) cells [10][11][12]. dpp expression is dynamic throughout embryogenesis, but it occurs primarily in two bands in late embryos: one located on the DME cells that depends on JNK pathway activation, and another in a ventral position that is independent of this pathway.…”