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 (scrib mutant). We show that the scrib mutation impacts the direct transcriptional output of the Notch pathway, without altering the global distribution of Su(H), the Notch dedicated transcription factor. The Notch-dependent neoplasms require however, the action of a group of transcription factors, similar to those previously identified for Ras/scrib neoplasm (namely AP-1, Stat92E, Ftz-F1, and bZIP factors), further suggesting the importance of this transcription factor network during neoplastic growth. Finally our work highlights some Notch/scrib specificities, in particular the role of the PAR domain containing bZIP transcription factor and Notch direct target Pdp1 for neoplastic growth.
Mechanisms underlying the cooperation between loss of epithelial polarity and Notch signaling during neoplastic growth in Drosophila
- Award Group:
- Funder(s): Agence Nationale de la Recherche
- Award Id(s): ANR-18-CE14-0041
- Funder(s):
- Award Group:
- Funder(s): Ligue Contre le Cancer
- Funder(s):
- Award Group:
- Funder(s): Fondation ARC pour la Recherche sur le Cancer
- Funder(s):
- Award Group:
- Funder(s): Medical Research Council
- Award Id(s): MR/L007177/1
- Funder(s):
- Award Group:
- Funder(s): European Union
- Award Id(s): PCIG13-GA-2013-618371
- Funder(s):
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Rémi Logeay, Charles Géminard, Patrice Lassus, Miriam Rodríguez-Vázquez, Diala Kantar, Lisa Héron-Milhavet, Bettina Fischer, Sarah J. Bray, Jacques Colinge, Alexandre Djiane; Mechanisms underlying the cooperation between loss of epithelial polarity and Notch signaling during neoplastic growth in Drosophila. Development 2022; dev.200110. doi: https://doi.org/10.1242/dev.200110
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