This leads to an ectopic furrow, marked itself by non-autonomous propagation of dpp expression. Our results indicate that pka C1 lies in a signalling pathway controlling the orderly temporal progression of differentiation across the eye disc. As induction of dpp expression is cell autonomous in pka C1 clones, and no direct induction of hh expression is observed, it appears that Pka C1 acts downstream or in a parallel pathway to hh. In Mad mutants the furrow initiation is blocked. To characterize Jun function in this process, dominant negative Jun mutants were expressed in specific precursor cells.
Flies expressing such mutant proteins show a dose-dependent loss of photoreceptors.
Furthermore, the transformation of cone cells to R7 neurons elicited by constitutively activating the Ras pathway is relieved in the presence of the Jun mutants. Ras-mediated activation of Jun was mimicked by mutating the serine and threonine phosphorylation sites in Jun to aspartic acid residues. A similar genetic strategy is being now used to identify other nuclear components of this cell fate decision that interact with Jun or are potential target genes. Ectopically expressed Svp disrupts the development of any other photoreceptor or the non-neuronal cone cells. Using this Svp-induced phenotype as an assay, we have performed genetic screens for modifiers of Svp function.