Abstract
To identify genes that modulate DER signaling in eye development, we undertook a genetic modifier screen in P line stock. gooseberry ( also know as gooseberry-distal, gsb-d ) is one of the four genes identified in this screen and defines a negative regulator of the DER signal pathway. We show that gsb mutations result in the failure of dorsal closure as the embryo exhibits a hole in the dorsal cuticle. Although ectopic expression of gsb has the similar cuticle phenotype as gsb mutants, the leading edge cells never elongate along the DV axis during stage 13; instead they stretch along the AP axis. Furthermore, overexpression of UAS-Gsb with pnr-GAL4 and eq-GAL4 induces a thorax cleft. The D.melanogaster Jun- N-terminal kinase ( DJNK ) signal transduction pathway, also know as stress-activated MAP kinases ( SAPK ), represent a third group of MAPK. In Drosophila, the JNK pathway is best known for its role in dorsal closure. In gsb mutant embryo, we observed the expansion of pucE69 enhancer trap expression into several rows of cells adjacent to the leading edge. In addition, we also found ectopic P-Tyr staining in lateral cells. In contrast, ectopic expression of gsb leads to a decrease in the expression of pucE69 in leading edge cells. Taken together our data indicate that gsb mutations result in the hyperactivation of DJNK signal, and overexpression of gsb result in downregulation of DJNK signal. Therefore, gsb may also be a negative regulator of the DJNK signal pathway during dorsal closure.