Abstract
Aggressive neoplastic growth can be initiated by a limited number of genetic alterations, such as the well-established cooperation between loss of cell architecture and hyperactive signaling pathways. However, our understanding of how these different alterations interact and influence each other remains very incomplete. Using Drosophila paradigms of imaginal wing disc epithelial growth, we have monitored the changes in Notch pathway activity according to the polarity status of cells and show that epithelial polarity changes directly impact the transcriptional output of the Notch pathway. Importantly, we show that this Notch pathway redirection is not mediated by a redeployment of Su(H), the Notch dedicated transcription factor, but relies on the cooperation with a combination of oncogenic transcription factors. Our work highlights in particular the role of the stress response CEBPG homologue CG6272/Irbp18 and of its partner Xrp1 suggesting that parts of the cellular competition program might promote neoplastic growth.