Drosophila Jun relays the Jun amino-terminal kinase signal transduction pathway to the Decapentaplegic signal transduction pathway in regulating epithelial cell sheet movement.

Abstract

We have characterized mutations in the Drosophila homolog of the mammalian proto-oncogene c-Jun gene (Djun). We demonstrate that DJUN in the embryo is a downstream target of the JNK signal transduction pathway during dorsal closure formation, and that the function of the JNK/DJUN pathway is to control the localized expression of decapentalegic (dpp), a member of the TGF.~ growth factor family. In contrast to previous observations, we find that both in the embryo and during photoreceptor cell determination, DJUN is not regulated by a pathway that involves MAPK.

Stress signaling in Drosophila

“…The JNK signaling pathway is required for morphogenesis in Drosophila Elements of the stress signaling pathway, speci®cally DJun, JNK, and JNKK, have been cloned and characterized in Drosophila over the last several years Hou et al, 1997;Kockel et al, 1997;Riesgo-Escovar et al, 1996;Sluss et al, 1996). These investigations have shown not only that the genes are present in the¯y and highly conserved at the sequence level in comparison to their mammalian counterparts, but also that they function in a concerted signal transduction pathway to regulate gene expression and cytoskeletal remodeling during embryogenesis.…”

“…One of the ®rst events is thought to be activation of the JNK signaling pathway in the LE cells. Members of the core JNK signaling module that have been cloned in Drosophila include hemipterous (hep), a JNKK and functional homolog of mammalian MKK7, basket (bsk), a JNK, and DJun Holland et al, 1997;Hou et al, 1997;Kockel et al, 1997;RiesgoEscovar et al, 1996;Sluss et al, 1996). Mutations in each gene lead to embryos with severe dorsal and anterior open cuticles indicative of a failure of DC and head involution.…”

“…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.…”

“…puc expression is similarly a ected. JNK pathway mutants also fail to accumulate the proper cytoskeletal network in LE cells and thus LE cells do not fully elongate dorsally (Hou et al, 1997;. 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.…”

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.…”