E ( y ) 1 / TAF 9 mediates the transcriptional output of Notch signaling 1 in Drosophila 2 3

15 Transcriptional activation of Notch signaling targets requires the formation of a ternary complex 16 that involves the intracellular domain of the Notch receptor (NICD), DNA-binding protein 17 Suppressor of Hairless [Su(H), RPBJ in mammals], and coactivator Mastermind (Mam). Here 18 we report that E(y)1/TAF9, a component of the transcription factor TFIID complex, interacts 19 specifically with the NICD/Su(H)/Mam complex to facilitate the transcriptional output of Notch 20 signaling. We identified E(y)1/TAF9 in a large-scale in vivo RNAi screen for genes involved in 21 a Notch-dependent mitotic-to-endocycle transition in Drosophila follicle cells. Knockdown of 22 e(y)1/TAF9 displayed Notch-like phenotypes and defects in target gene and activity reporter 23 expression in both the follicle cells and wing imaginal discs. Epistatic analyses in these two 24 tissues indicate that E(y)1/TAF9 functions downstream of the Notch cleavage. Biochemical 25 studies in S2 cells demonstrated that E(y)1/TAF9 physically interacts with the transcriptional 26 effectors of Notch signaling, Su(H) and NICD. Together, our data suggest that the association of 27 the NICD/Su(H)/Mastermind complex with E(y)1/TAF9 in response to Notch activation recruits 28 the transcription initiation complex to induce Notch target genes, coupling Notch signaling with 29 the transcriptional machinery. 30 31