ArticleJournal of cell science2014
E(y)1/TAF9 mediates the transcriptional output of Notch signaling in Drosophila.
Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Step-brothers in arms, SAGA and ATAC co-activator complexes, use different strategies.The EMBO journal · 2026Review
- Set1 promotes Notch-induced transcriptional activation.Cellular and molecular life sciences : CMLS · 2026Article
- The Ubiquitin Conjugating Enzyme UbcD1 is Required for Notch Signaling Activation DuringFrontiers in genetics · 2021Article
- Activation of TAF9Frontiers in pharmacology · 2021Article
- Distinct gene-selective roles for a network of core promoter factors inBiology open · 2019Article
- Drosophila TRF2 and TAF9 regulate lipid droplet size and phospholipid fatty acid composition.PLoS genetics · 2017Article
- The SWI/SNF Complex Protein Snr1 Is a Tumor Suppressor inCancer research · 2017Article
- The Ecdysone and Notch Pathways Synergistically Regulate Cut at the Dorsal-Ventral Boundary in Drosophila Wing Discs.Journal of genetics and genomics = Yi chuan xue bao · 2016Article
- A large-scale in vivo RNAi screen to identify genes involved in Notch-mediated follicle cell differentiation and cell cycle switches.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Transcriptional activation of Notch signaling targets requires the formation of a ternary complex that involves the intracellular domain of the Notch receptor (NICD), DNA-binding protein Suppressor of Hairless [Su(H), RPBJ in mammals] and coactivator Mastermind (Mam). Here, we report that E(y)1/TAF9, a component of the transcription factor TFIID complex, interacts specifically with the NICD-Su(H)-Mam complex to facilitate the transcriptional output of Notch signaling. We identified E(y)1/TAF9 in a large-scale in vivo RNA interference (RNAi) screen for genes that are involved in a Notch-dependent mitotic-to-endocycle transition in Drosophila follicle cells. Knockdown of e(y)1/TAF9 displayed Notch-mutant-like phenotypes and defects in target gene and activity reporter expression in both the follicle cells and wing imaginal discs. Epistatic analyses in these two tissues indicated that E(y)1/TAF9 functions downstream of Notch cleavage. Biochemical studies in S2 cells demonstrated that E(y)1/TAF9 physically interacts with the transcriptional effectors of Notch signaling Su(H) and NICD. Taken together, our data suggest that the association of the NICD-Su(H)-Mastermind complex with E(y)1/TAF9 in response to Notch activation recruits the transcription initiation complex to induce Notch target genes, coupling Notch signaling with the transcription machinery.
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