Fig. 3.
Effect of Slpr transgene expression on embryonic JNK target gene expression and tissue closure. (A) lacZ expression from the JNK-dependent pucE69 enhancer trap in embryos expressing the indicated Slpr transgenes with pnr-G4. Images are lateral views of three segments of stage 14 embryos focusing on the leading edge of the dorsal ectoderm. Dominant negative activity reduces the number of cells with active JNK signaling and puc-lacZ expression (c,d,e,h,j). Some transgenes have no effect (g,i), whereas others activate signaling, increasing the intensity and extent of lacZ expression (b,f,k,l). Scale bar: 10 μm. (B) Thr295 in the activation segment of Slpr kinase is essential for function. (a-e) Dorsolateral views of stage 16 embryos stained for Fasciclin III, revealing the ectodermal epithelium and extent of dorsal closure. Scale bar: 20 μm. (C) The effect of expression of Slpr transgenes, using pnr-G4, on the adult thorax morphology parallels the effect of transgene expression in the embryo. Dominant negative transgenes produce midline thorax clefts and widening of the space between adjacent dorsocentral bristles (a,d,g) compared with no transgene controls (b). Hyperactive Slpr variants promote loss of midline tissue, such as the scutellum, and narrowing of the inter-bristle space (c,f,i).