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1/TAF9 Mediates the Transcriptional Output of Notch Signaling In ß 2014. Published by The Company of Biologists Ltd | Journal of Cell Science (2014) 127, 3830–3839 doi:10.1242/jcs.154583 RESEARCH ARTICLE E(y)1/TAF9 mediates the transcriptional output of Notch signaling in Drosophila Gengqiang Xie1, Zhongsheng Yu2, Dongyu Jia1, Renjie Jiao1,* and Wu-Min Deng1,* ABSTRACT cells, interaction between TRF3 and TAF3 is essential for hematopoiesis (Ba´rtfai et al., 2004; Hart et al., 2007; Hart et al., Transcriptional activation of Notch signaling targets requires the 2009). Kalogeropoulou et al. have demonstrated that TAF4b is formation of a ternary complex that involves the intracellular domain specifically associated with c-Jun and other AP-1 family of the Notch receptor (NICD), DNA-binding protein Suppressor of members to regulate the expression of Integrin a6 in the Hairless [Su(H), RPBJ in mammals] and coactivator Mastermind context of cancer progression (Kalogeropoulou et al., 2010). (Mam). Here, we report that E(y)1/TAF9, a component of the Although a recent report has shown that TAF4 interacts with transcription factor TFIID complex, interacts specifically with the Pygopus, a transcriptional activator of Wingless (Wg) signaling, NICD–Su(H)–Mam complex to facilitate the transcriptional output of to induce transcription of naked cuticle in Drosophila (Wright Notch signaling. We identified E(y)1/TAF9 in a large-scale in vivo and Tjian, 2009), how other signaling pathways, such as Notch, RNA interference (RNAi) screen for genes that are involved in a are regulated by specific TAFs is poorly understood. Notch-dependent mitotic-to-endocycle transition in Drosophila Notch signaling is an evolutionally conserved pathway across follicle cells. Knockdown of e(y)1/TAF9 displayed Notch-mutant- species that plays a pivotal role in many different developmental like phenotypes and defects in target gene and activity reporter events, including cell fate determination, control of cell expression in both the follicle cells and wing imaginal discs. proliferation and apoptosis, and the maintenance of stem cells Epistatic analyses in these two tissues indicated that E(y)1/TAF9 (Artavanis-Tsakonas and Muskavitch, 2010; Guruharsha et al., functions downstream of Notch cleavage. Biochemical studies in S2 2012; Tien et al., 2009). Dysregulation of Notch is implicated in a cells demonstrated that E(y)1/TAF9 physically interacts with the number of diseases, including cancer (Louvi and Artavanis- transcriptional effectors of Notch signaling Su(H) and NICD. Taken Tsakonas, 2012; Ntziachristos et al., 2014). Notch signaling together, our data suggest that the association of the NICD–Su(H)– activation is mediated by a direct interaction between the Notch Mastermind complex with E(y)1/TAF9 in response to Notch receptor in one cell and its ligand on the neighboring cell (Diaz- activation recruits the transcription initiation complex to induce Benjumea and Cohen, 1995; Doherty et al., 1996). Such an Notch target genes, coupling Notch signaling with the transcription interaction induces two consecutive proteolytic processes that machinery. result in the release of the Notch intracellular domain (NICD) (Struhl and Adachi, 1998), which is then translocated to the KEY WORDS: E(y)1, TAF9, Notch pathway, Drosophila, TFIID nucleus and activates transcription of its target genes by complex, Transcriptional regulation interacting with the DNA-binding protein Suppressor of Hairless [Su(H)] and the coactivator Mastermind (Mam) to INTRODUCTION form a functional Su(H)–NICD–Mam ternary complex (Bailey The eukaryotic transcription factor IID (TFIID) complex, and Posakony, 1995; Lecourtois and Schweisguth, 1995). comprising the TATA box-binding protein (TBP) and 13 or 14 Although numerous Notch target genes have been identified in TBP-associated factors (TAFs), plays an essential role in the different tissues or organs during different developmental stages, transcriptional regulation of gene expression, and all components how the Su(H)–NICD–Mam ternary complex regulates their of this complex were generally thought to be required for RNA- expression is largely unclear. Recent findings in different systems polymerase-II-initiated transcription in all eukaryotic cells have suggested that chromatin-associated epigenetically- (Goodrich and Tjian, 2010; Thomas and Chiang, 2006). regulatory mechanisms are very important for proper expression However, an increasing number of studies suggest that some of Notch target genes (Bray et al., 2005; Domanitskaya and TAFs found in different species are vital in specific events, such Schu¨pbach, 2012; Endo et al., 2011; Kugler and Nagel, 2007; as apoptosis, spermatogenesis and adipogenesis (Goodrich and Mulligan et al., 2011; Yu et al., 2013; Zeng et al., 2013). In flies, Tjian, 2010). For example, mouse TAF7L is specifically required histone chaperones Asf1 and Nap1 are differentially associated for male germ-cell differentiation (Cheng et al., 2007; Pointud with LID-associated factor (LAF) and RPD3-LID-associated et al., 2003), and, in both zebrafish and mouse embryonic stem factor (RLAF) silencing complexes to mediate epigenetic silencing at the Notch target Enhancer of Split [E(spl)] cluster (Moshkin et al., 2009). A SIRT1–LSD1 co-repressor complex 1Department of Biological Science, Florida State University, Tallahassee, FL 32304-4295, USA. 2State Key Laboratory of Brain and Cognitive Science, Institute regulates Notch target gene expression in both mammalian and of Biophysics, the Chinese Academy of Sciences, Datun Road 15, Beijing Drosophila cultured cells (Mulligan et al., 2011). Our very recent 100101, China. study has demonstrated that the histone chaperone CAF-1 *Authors for correspondence ([email protected]; [email protected]) complex epigenetically and positively regulates Notch target gene expression in Drosophila (Yu et al., 2013). But the most Received 4 April 2014; Accepted 23 June 2014 basic questions of how the Su(H)–NICD–Mam complex activates Journal of Cell Science 3830 RESEARCH ARTICLE Journal of Cell Science (2014) 127, 3830–3839 doi:10.1242/jcs.154583 expression of Notch target genes and which cofactor(s) bring it to 2011) (both referred to as RNAi) under the control of the the general transcription machinery are unanswered. upstream activating site (UAS). These lines were crossed to the The Drosophila egg chamber is an ideal system to study flip-out Gal4 driver (Ito et al., 1997; Pignoni and Zipursky, 1997) the regulation of Notch signaling and its developmental to generate random follicle-cell RNAi clones that were marked by consequences (Bastock and St Johnston, 2008; Klusza and Deng, the expression of green and red fluorescent proteins (GFP and 2011). During mid-oogenesis (stages 7–10A), Notch signaling is RFP, respectively). The follicle-cell RNAi clones were then activated in entire follicular epithelia by the germline-expressed screened for defects in the expression pattern of the negative ligand, Delta (Dl) (Deng et al., 2001; Lo´pez-Schier and St Notch target Cut, a homeodomain-containing transcription factor Johnston, 2001). This activation induces the follicle cells from the (Sun and Deng, 2005). Cut is normally expressed in early mitotic cycle into endoreplication, which is mediated by the oogenesis (stages 1–6) and then downregulated at stage 7 upon suppression of Cut and activation of Hindsight (Hnt; also known as Notch activation in follicle cells (Sun and Deng, 2005). Failure to Pebbled) through Notch signaling (Sun and Deng, 2007; Sun and downregulate Cut at stage 7 suggests a defect in Notch signaling. Deng, 2005). As in other processes, this Notch-dependent cell From this screen, we found that knockdown of the gene CG6474 cycle transition also requires Notch protein cleavage, which is [enhancer of yellow 1 (e(y)1)], which encodes a homolog of achieved by c-secretase components Presenilin and Nicastrin. TAF9, a core component of the TFIID transcription initiation In addition, the nuclear effector of Notch signaling Su(H) is complex (Soldatov et al., 1999; Thomas and Chiang, 2006), needed for the switch. The precise timing of Notch signaling resulted in prolonged Cut expression in 74% (n572) of follicle during mid-oogenesis is regulated through multiple mechanisms cell RNAi clones at stages 7–8 (Fig. 1A), suggesting a Notch (Domanitskaya and Schu¨pbach, 2012; Heck et al., 2012; Poulton defect in e(y)1-depleted follicle cells. et al., 2011). Our recent finding demonstrated that the microRNA To confirm that E(y)1 is required for Notch signaling in follicle pathway regulates the temporal pattern of Notch signaling by cells, we examined the expression of zinc-finger protein Hnt, a repressing Delta-mediated inhibition of Notch in Drosophila positive follicle-cell-specific Notch target, which is normally follicle cells (Poulton et al., 2011). Interestingly, transcriptional expressed in the entire follicular epithelium from stages 7–10A cofactors are also involved in precise control of Notch signaling (Sun and Deng, 2007). Downregulation of Hnt in mid-oogenesis (Domanitskaya and Schu¨pbach, 2012; Heck et al., 2012) – the transcriptional co-repressor SMRTER inhibits Notch activity in a temporally restricted manner in follicular epithelium (Heck et al., 2012), whereas the transcriptional cofactor Corepressor for element-1-silencing transcription factor (CoREST) promotes Notch signaling in a spatially restricted manner by affecting histone H3 K27 tri-methylation and histone H4 K16 acetylation in the follicle cells (Domanitskaya and Schu¨pbach, 2012). In a genetic RNA
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