PT  - JOURNAL ARTICLE
AU  - Rémi Logeay
AU  - Charles Géminard
AU  - Patrice Lassus
AU  - Diala Kantar
AU  - Lisa Héron-Milhavet
AU  - Bettina Fischer
AU  - Sarah J. Bray
AU  - Jacques Colinge
AU  - Alexandre Djiane
TI  - Loss of epithelial polarity redirects Notch signaling and triggers a Xrp1 response during neoplastic growth in <em>Drosophila</em>
AID  - 10.1101/2020.02.07.938621
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.02.07.938621
4099  - http://biorxiv.org/content/early/2020/02/07/2020.02.07.938621.short
4100  - http://biorxiv.org/content/early/2020/02/07/2020.02.07.938621.full
AB  - 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. We further provide evidence that this Notch redirection is not mediated by new genomic binding regions for Su(H), but relies on the cooperation with Su(H) of 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 cellular competition, or parts of the cellular competition program, are co-opted during neoplastic growth.