Abstract
RUGOSE (RG): encodes an A kinase anchor protein and was isolated as a genetic interactor of the Notch and epidermal growth factor receptor (EGFR) pathways during eye development in Drosophila. rg mutants display a small, rough eye phenotype primarily caused by the loss of cone cells. Here we show that the basis of this phenotype is cell type-specific apoptosis rather than transformation and hence can be rescued by reduction of proapoptotic signals. Moreover, a nearly complete rescue is observed by an increased Notch signal suggesting an antiapoptotic function of Notch in this developmental context. Cone cell loss in rg mutants is accompanied by enhanced Jun N-terminal kinase activity and, concomitantly, by a reduction of EGFR signalling activity. Together, these findings support the idea that rg plays an important role in the integration of different signals required for the exact regulation of cone cell development and survival.
