Over-expression of <i>scarface</i> mimics the loss of Egfr pathway activity.

<p>(A-B) Embryos hybridized using a digoxigenin-labeled RNA probe for <i>dpp</i> (blue). Over-expression of <i>scaf</i> brings about a reduction in <i>dpp</i> expression (A) whereas <i>dpp</i> expression expands in <i>scaf</i> mutant embryos (B), similarly to loss- and gain-of-function mutations in the Egfr pathway, respectively. (C-F) Embryos stained for pMad (red). (C, D) In keeping with <i>dpp</i> expression levels, pMad staining decreases upon <i>scaf</i> over-expression (C), and is augmented in a <i>scaf</i> mutant (D). (E, F) Although pMad staining is reduced in <i>rhomboid</i> single mutant embryo (E), it expands in embryo doubly mutant for <i>scaf</i> and <i>rhomboid</i> (F), as in <i>scaf</i> single mutant (D), indicating that <i>scaf</i> is epistatic to <i>Egfr</i> signaling. (G-H) Model showing how Egfr signaling in the lateral epidermis positively and non-autonomously contributes to JNK pathway activity in LE cells and to DC. (G) The Egfr pathway normally acts in the lateral epidermis to prevent expression of the JNK antagonist, <i>scaf</i>, thus supporting maximal JNK activity in LE cells. (H) When Egfr signaling is defective, deregulated Scaf subsequently attenuates functional JNK signaling in LE cells, thus hindering the process of DC. Bold text and arrows/bars indicate normal levels of gene expression and regulation, whereas gray fonts designate abnormally lower levels of expression and regulation, respectively.