JNK signaling and morphogenesis in Drosophila

The recent focus on Drosophila mutants with a dorsal hole has yielded valuable insights into the mechanisms underlying epithelial movements during development. Dorsal closure, the process affected in these genetically pierced embryos, is controlled by the Drosophila JNK pathway, equivalent to the mammalian stress-activated MAPK pathway. During dorsal closure, activation of JNK signaling is restricted to the leading edges of the migrating dorsal ectoderm. In these cells, the Drosophila JNKK/JNK/JUN cascade induces TGF-β/dpp expression, resulting in the patterning and movement of the neighboring lateral ectodermal cells. Coupling of MAPK/TGF-β signaling pathways emerges as a conserved mechanism for cell migration in related processes like wound repair and invasiveness. The recent focus on Drosophila mutants with a dorsal hole has yielded valuable insights into the mechanisms underlying epithelial movements during development. Dorsal closure, the process affected in these genetically pierced embryos, is controlled by the Drosophila JNK pathway, equivalent to the mammalian stress-activated MAPK pathway. During dorsal closure, activation of JNK signaling is restricted to the leading edges of the migrating dorsal ectoderm. In these cells, the Drosophila JNKK/JNK/JUN cascade induces TGF-β/dpp expression, resulting in the patterning and movement of the neighboring lateral ectodermal cells. Coupling of MAPK/TGF-β signaling pathways emerges as a conserved mechanism for cell migration in related processes like wound repair and invasiveness.