ライフサイエンスコーパス: TFIID

1 TFIID assists in nucleating PIC formation, completed by

2 TFIID binds promoter DNA to recruit RNA polymerase II an

3 TFIID comprises the TATA-binding protein (TBP) and 13 TB

4 TFIID depletion can be complemented in vitro by addition

5 TFIID is recruited to the promoter through DTIE but is d

6 TFIID, a megadalton-sized multiprotein complex comprisin

7 TFIID-a complex of TATA-binding protein (TBP) and TBP-as

8 Although Taf14 is not conserved as a TFIID subunit in metazoans, it is conserved through its

9 These results establish a TFIID requirement for RNAPII pausing and suggest pause r

10 at the SAGA Taf and Taf-like subunits form a TFIID-like core complex at the center of SAGA that makes

11 myotubes, the cells undergo a switch from a TFIID-based transcription system to a TRF3-TAF3-based sy

12 clude that TAF7, until now considered only a TFIID component and regulator of TAF1-dependent transcri

13 clearly define the human Pol II promoter: a TFIID binding site with built-in downstream information

14 yeast TFIIA in the integration of activator-TFIID contacts with promoter conformation and downstream

15 tep toward structurally dissecting activator/TFIID interactions, we determined the three-dimensional

16 in the presence of a taf1 mutation affecting TFIID activity that otherwise blocks HO transcription.

17 Although TFIID may also function as a coactivator through direct

18 lt of ablated interactions between d3-10 and TFIID and mediator.

19 ed SAGA (Spt-Ada-Gcn5-acetyltransferase) and TFIID (Transcription factor-IID)-dependent mechanisms of

20 rearrangements of enhancer-promoter DNA and TFIID-bound TFIIA.

21 We show that promoters of SAGA-dominated and TFIID-dominated genes can be statistically distinguished

22 new insights into the roles of HNF4alpha and TFIID in RNA polymerase II transcription.

23 ochemical studies have shown that Pol II and TFIID (transcription factor IID) contact overlapping reg

24 but dispensable for Taf-Taf interactions and TFIID stability.

25 tor required for Sp1 activation/Mediator and TFIID complexes at both the RNA and protein level, and t

26 re consistent with a model in which PRC1 and TFIID could co-occupy genes poised for activation during

27 upts the binding of TATA binding protein and TFIID, components of the preinitiation complex.

28 Prior studies suggested that SAGA and TFIID are alternative factors that promote RNA polymeras

29 st different implementations of the SAGA and TFIID assembly pathways that may depend upon whether a s

30 n and the relative contributions of SAGA and TFIID at genes regulated by both complexes have not been

31 Genome-wide mapping of SAGA and TFIID found binding of both factors at many genes indepe

32 revisit fundamental questions about SAGA and TFIID function in yeast.

33 hereas heat shock genes utilize the SAGA and TFIID pathways rapidly and in parallel.

34 by CBP/p300 and SRC-3 dismissal and SAGA and TFIID stabilization/recruitment.

35 zation of a gene that requires both SAGA and TFIID.

36 ith the previous classification of SAGA- and TFIID-dominated genes.

37 actors could differentiate between SAGA- and TFIID-dominated promoters.

38 nding of both TATA binding protein (TBP) and TFIID to the TATA box of core promoters and ICP4 has bee

39 ze in vivo the association of M1BP, TRF2 and TFIID subunit, TAF1.

40 TAF7, another TFIID subunit, binds TAF1 and inhibits TAF1 HAT activity

41 onstrated that promoters of both classes are TFIID dependent, in agreement with recent in vivo findin

42 start sites were positionally constrained at TFIID-engaged downstream +1 nucleosomes.

43 pon depletion of Kin28 is more pronounced at TFIID-dominated promoters compared to SAGA-dominated pro

44 ion with BTAF1, hence the formation of the B-TFIID complex, and its dynamic cycling on and off of DNA

45 the division of promoter dependence between TFIID and SAGA.

46 est a mechanism for how interactions between TFIID, TFIIA, and Rap1 contribute to the high rate of tr

47 atistical PIC preferences of binding to both TFIID-dominated and SAGA-dominated genes correlate with

48 Thus, RNR3 is dependent upon both TFIID and SAGA, two complexes that deliver TATA-binding

49 , we find that TFIID is associated with both TFIID- and SAGA-dependent genes and that TFIID and Media

50 g arrests an isomerization of promoter-bound TFIID that is required for the engagement of Pol II duri

51 cription factors rapidly bind promoter-bound TFIID-TFIIA, after which complexes undergo a slow isomer

52 TFIIB, and TFIIF assemble on promoter-bound TFIID-TFIIA.

53 PIC assembly is nucleated by TFIID, a complex composed of the TATA-binding protein (T

54 from transcription, and mediated in part by TFIID.

55 he Inr (initiator), but is not recognized by TFIID and cannot function in lieu of an Inr.

56 tes TBPL2 does not assemble into a canonical TFIID complex.

57 ernative core factor TAF3, but not canonical TFIID subunits, away from the nuclear periphery, where t

58 sociated with PCAF rather than the canonical TFIID complex.

59 complex is required to replace the canonical TFIID to recapitulate MyoD-dependent activation of Myoge

60 Replacement of the canonical TFIID-TBP complex with TRF3/TBP2 was reported to be requ

61 results thus have implications for cellular TFIID assembly and suggest a novel regulatory state for

62 of TFIID by rapid depletion of S. cerevisiae TFIID subunits and measurement of changes in nascent tra

63 nding to a known transcriptional coactivator TFIID-binding target, Taf5.

64 uence properties and use of the coactivators TFIID or SAGA.

65 e II transcription initiation factor complex TFIID.

66 ltisubunit core promoter recognition complex TFIID in vivo requires knowledge of how individual subun

67 ole in the core promoter recognition complex TFIID, genome-wide binding studies reveal that TAF3 loca

68 nit of the core promoter recognition complex TFIID.

69 and the histone fold (HF) domain-containing TFIID subunits TAF11 and TAF13.

70 ng complex, and TAF1, an element of the core TFIID transcriptional machinery.

71 tions dictate TAF2 incorporation into a core-TFIID complex that exists in the nucleus.

72 ed RNA polymerase II transcription factor D (TFIID) complex is composed of TATA box-binding protein (

73 eins is shared in transcription factor II D (TFIID) and SAGA transcription regulatory complexes.

74 a liver-specific transcription factor II D (TFIID) defect in transcription initiation.

75 Transcription factor II D (TFIID) is a multiprotein complex that nucleates formatio

76 ng purified PRC1, transcription factor II D (TFIID), and Mediator indicate that PRC1 blocks the recru

77 nanoscale information on activator-dependent TFIID assembly and transcription initiation.

78 Here, biochemical studies show a direct TFIID-E-protein interaction that (1) is mediated through

79 of the genome can be characterized as either TFIID- or SAGA-dominant, it is expected that many genes

80 g their poor incorporation within endogenous TFIID.

81 n, and (3) mechanistically acts by enhancing TFIID binding to the core promoter.

82 Pol II initiation complex and then exchanges TFIID for complexes containing ELL/EAF and P-TEFb to fac

83 as well as a mechanism involving facilitated TFIID binding through direct interaction with an E-prote

84 plex versus the housekeeping assembly factor TFIID.

85 ctor proteins that include initiation factor TFIID.

86 omplex, as well as general initiation factor TFIID.

87 The transcription factor TFIID components TAF7 and TAF1 regulate eukaryotic trans

88 The general transcription factor TFIID comprises the TATA-box-binding protein (TBP) and a

89 General transcription factor TFIID is a cornerstone of RNA polymerase II transcriptio

90 General transcription factor TFIID is a key component of RNA polymerase II transcript

91 is dominated by either transcription factor TFIID or SAGA.

92 The general transcription factor TFIID recognizes specifically the core promoter of genes

93 d Taf1 for a subunit of transcription factor TFIID that serves as a multifunctional transcriptional r

94 pted the binding of the transcription factor TFIID, the major component of the pre-initiation complex

95 A polymerase II general transcription factor TFIID.

96 ol II) and the general transcription factors TFIID, TFIIA, TFIIB, TFIIF, TFIIE, and TFIIH.

97 ndependently of the tail module and favoring TFIID-regulated genes.

98 ap1 requires TAF(II)s, suggesting a role for TFIID in stabilizing activator binding in vivo.

99 genes, such as RPS5, RPL2B, and RPS11B, for TFIID recruitment to initiate transcription, and the rec

100 sses and better defines the binding site for TFIID and is surprisingly invariant over a wide range of

101 at DTIE does not serve as a docking site for TFIID, the major core promoter-binding factor.

102 bly and suggest a novel regulatory state for TFIID function.

103 interaction with TFIID but is released from TFIID upon transcription initiation.

104 Release of TAF7 from TFIID by TAF1 phosphorylation of TAF7 increased TAF1 HAT

105 well as general transcription factors (e.g., TFIID, TFIIB, and Mediator) for antisense transcription

106 factors that govern Pol II initiation (e.g., TFIID, TFIIH, and Mediator), pausing, and elongation (e.

107 that H3K4me3-TAF3 interactions direct global TFIID recruitment to active genes, some of which are p53

108 Here we describe a heterotrimeric TFIID subcomplex consisting of the TAF2, TAF8 and TAF10

109 Local promoter-proximal HNF4A-TFIID interactions therefore act as instructive signals

110 systematic characterization of the HNF4alpha-TFIID link revealed that the HNF4alpha DNA-binding domai

111 By generating altered holo-TFIID complexes in Drosophila we identify the ETO domain

112 were observed when each activator binds holo-TFIID.

113 a stepwise assembly pathway of nuclear holo-TFIID, regulated by nuclear import of preformed cytoplas

114 signals with real-time interactions of holo-TFIID molecules at individual DNA templates.

115 Human TFIID is a megadalton-sized complex comprising TATA-bind

116 How human TFIID-a megadalton-sized multiprotein complex composed o

117 Here we present the structure of human TFIID in complex with TFIIA and core promoter DNA, deter

118 electron microscopy (EM) to visualize human TFIID with promoter DNA.

119 The size and complexity of Pol II, TFIID, and TFIIH have precluded their reconstitution fro

120 xamined changes in transcription factor IID (TFIID) and cofactor required for Sp1 activation/Mediator

121 a component in the transcription factor IID (TFIID) complex.

122 The general transcription factor IID (TFIID) plays a central role in the initiation of RNA pol

123 Transcription factor IID (TFIID) plays a key role in regulating eukaryotic gene ex

124 The largest transcription factor IID (TFIID) subunit, TBP-associated factor 1 (TAF1), possesse

125 nsferase)(1,2) and transcription factor IID (TFIID)(2-4).

126 Transcription factor IID (TFIID), the TBP-containing coactivator that functions at

127 ha (HNF4alpha) and transcription factor IID (TFIID).

128 a gene-specific role for the TAFH domain in TFIID recruitment and activation of a large subset of ge

129 nd its TBP-interacting region are similar in TFIID, whereas Taf5 and the Taf6 HEAT domain adopt disti

130 reagent for determining the role of Taf14 in TFIID function.

131 of the transcriptional complex that includes TFIID, ICP4, ICP27, and ICP22.

132 hese general transcription factors including TFIID, BAF, and Mediator may facilitate global changes i

133 studies reveal that TAF4b incorporation into TFIID induces an open conformation at the lobe involved

134 r defects in transcription of two TATA-less, TFIID-dependent genes.

135 00 target regions that include highly likely TFIID binding sites.

136 icate that p53 dynamically escorts and loads TFIID onto its target promoters.

137 bsence of NuA4, ribosomal protein genes lose TFIID dependency and become SAGA dependent for transcrip

138 e functions of the TAF subunits of mammalian TFIID in physiological processes remain poorly character

139 important for the heterodimerization of many TFIID subunits.

140 Using the same approach to map TFIID, we find that TFIID is associated with both TFIID-

141 ying a potential role for Taf14 in mediating TFIID-chromatin interactions.

142 utionarily conserved IDR within the metazoan TFIID transcription complex.

143 The multisubunit TFIID plays a direct role in transcription initiation by

144 In addition, purified Taf2-DeltaC mutant TFIID is devoid of Taf14, making this variant a powerful

145 either Mediator, the activator Gal4-V16, nor TFIID specifically compensate for the low transcription

146 blocks the recruitment of Mediator, but not TFIID.

147 Notably, TFIID's interaction with DNA induces p53 to rapidly diss

148 reviously proposed, with limiting amounts of TFIID-TBP being required to promote muscle-specific gene

149 TAF-4, a component critical for assembly of TFIID and the pol II preinitiation complex.

150 bridges the TBP-TATA complex with lobe B of TFIID.

151 gly, we found that while promoter binding of TFIID and TFIIA is stable, promoter binding by TFIIB is

152 The stabilized binding of TFIID by TFIIA may in turn allow ICP4 to more efficientl

153 IA were required to stabilize the binding of TFIID to the INR-mutated late promoter.

154 TFIIA's ability to stabilize the binding of TFIID to the TATA box.

155 the hierarchal promoter-specific binding of TFIID, TFIIA, and TFIIB.

156 equestering TAF-4, an essential component of TFIID.

157 These included 11 components of TFIID and 4 components of the Mediator complex.

158 required for interactions with components of TFIID and mediator and, as a consequence, are necessary

159 ggest that ICP4 interacts with components of TFIID and Mediator in the context of viral infection, an

160 as not found in complexes with components of TFIID and mediator, suggesting that the defect in RNA po

161 ors can interact with multiple components of TFIID, it is unknown whether common or distinct surfaces

162 ce suggests that the role and composition of TFIID are more diverse than previously understood.

163 e the effects of changing the composition of TFIID in a simple system, we depleted TATA box-binding p

164 on with extracts made from cells depleted of TFIID subunit Taf1 demonstrated that promoters of both c

165 -containing promoters, which are depleted of TFIID, a +1 nucleosome was positioned to be in competiti

166 have revealed significant downregulation of TFIID subunits in terminally differentiated myocytes, he

167 act may induce unique structural features of TFIID, thus providing nanoscale information on activator

168 ucturally and functionally distinct forms of TFIID suggests that the different conformers may serve a

169 nits contribute to the essential function of TFIID are only poorly understood.

170 actors, showing the overlapping functions of TFIID and SAGA at this gene set.

171 f H4) promotes transcriptional initiation of TFIID (a complex of TBP and TBP-associated factors [TAFs

172 The magnitude of TFIID dependence varies with growth conditions, although

173 re importantly, uncover a novel mechanism of TFIID recruitment and gene activation.

174 provide a strategy to dissect mechanisms of TFIID function in vivo.

175 pausing upon acute depletion (t = 60 min) of TFIID subunits in human or Drosophila cells.

176 developmental stage-specific organization of TFIID or SAGA complexes, in unicellular genomes, however

177 Here we report that TAF7L, a paralogue of TFIID subunit TAF7, is enriched in adipocytes and white

178 moter recognition complex takes the place of TFIID in adult hepatocytes and to uncover the mechanisms

179 omena that are linked to the potentiation of TFIID(4-6) interactions with H3K4me3.

180 reduced free energy compared to promoters of TFIID-dominated genes.

181 n a Deltaeaf1 strain depletes recruitment of TFIID (a TAF-dependent form of TBP) but not the TAF-inde

182 otein genes to facilitate the recruitment of TFIID for transcriptional stimulation, hence providing a

183 initiation in part by aiding recruitment of TFIID to the promoter.

184 he conserved additional C-terminal region of TFIID subunit TAF6 can be divided into two domains: a sm

185 We re-examined the role of TFIID by rapid depletion of S. cerevisiae TFIID subunits

186 ides novel insights into the general role of TFIID in promoter recognition, PIC assembly, and transcr

187 Consistent with the role of TFIID in promoting gene expression, RNA-seq of wild-type

188 tates the formation of a rearranged state of TFIID that enables promoter recognition and binding.

189 and what changes if any in the structure of TFIID may occur upon binding activators.

190 termined the three-dimensional structures of TFIID bound to three distinct activators (i.e., the tumo

191 gh the TATA-binding protein (TBP) subunit of TFIID is necessary and sufficient for in vitro transcrip

192 on in mice, we show that the TAF4 subunit of TFIID is required for post-natal hepatocyte maturation.

193 e Rap1 binding domain of the Taf4 subunit of TFIID.

194 nding protein-associated factor) subunits of TFIID alter the kinetic mechanism by which complexes ass

195 mains in histone fold-containing subunits of TFIID and of co-activator SAGA are important for the ass

196 moter and that the TAF6 and TAF9 subunits of TFIID appear to be in close proximity to the MTE.

197 tively the Taf4, Taf5, and Taf12 subunits of TFIID represent the physical and functional targets for

198 ors 1 and 7 (TAF1 and TAF7), two subunits of TFIID, are integral to the regulation of eukaryotic tran

199 Here we show that two subunits of TFIID, Taf1 and Taf4, similarly show increased occupancy

200 omoter elements are contacted by subunits of TFIID, with TAF1 and TAF2 mediating major interactions w

201 ver, the understanding in molecular terms of TFIID assembly and function remains poorly understood.

202 egulation of RNR3 and contrast it to that of TFIID.

203 ates that differ by a 100 A translocation of TFIID's lobe A.

204 of nearly all mRNAs is strongly dependent on TFIID function.

205 AL10 antisense transcription is dependent on TFIID, its sense transcription does not require TFIID.

206 n part to differential dependence on SAGA or TFIID.

207 pective of previous designations of SAGA- or TFIID-dominated genes.

208 through this interaction, can target TBP or TFIID to promoters containing HNF4alpha-binding sites in

209 P4 to stabilize the binding of either TBP or TFIID to the TATA box of representative early, late, and

210 Surprisingly, no TFIIB or TFIID was detectable or functionally required at the ini

211 TAF14 but not by overexpression of any other TFIID subunit.

212 occurs preferentially at SAGA-regulated over TFIID-regulated genes on a genome-wide scale.

213 ng with Mediator, but leaves TBP and perhaps TFIID intact, highlighting a specific mechanism for PRC1

214 ure/function relationships of the prototypic TFIID versus 4b/4-IID, we have compared their 3D structu

215 hat the MTE promotes the binding of purified TFIID to the core promoter and that the TAF6 and TAF9 su

216 of assemblies generated with purified Rap1, TFIID, and TFIIA on RPG enhancer-promoter DNA indicate t

217 s, which we interpret to reflect native Rap1-TFIID interactions.

218 RPG enhancer-promoter DNA indicate that Rap1-TFIID interaction induces dramatic conformational rearra

219 IID-dependent' are highly sensitive to rapid TFIID depletion and insensitive to rapid SAGA depletion.

220 s that are generally more sensitive to rapid TFIID depletion.

221 t by targeting the core promoter recognition TFIID complex and aiding in its recruitment to promoter

222 to uncover the mechanisms that down-regulate TFIID during this critical developmental transition.

223 ID, its sense transcription does not require TFIID.

224 on of yeast ribosomal protein genes requires TFIID and the DNA-binding transactivator Rap1.

225 erved coactivator complexes, Mediator, SAGA, TFIID, and NuA4.

226 t involving SAGA and then involving a slower TFIID recruitment, whereas heat shock genes utilize the

227 ith in vitro studies, we found that specific TFIID subunits, in addition to cross-linking at the core

228 ssed by overexpression of the yeast-specific TFIID subunit TAF14 but not by overexpression of any oth

229 functional INR, ICP4 can no longer stabilize TFIID binding to the TATA box of the late promoter and r

230 s TFIID's ability to bind DNA by stabilizing TFIID contacts with both the core promoter and a region

231 TAF7 is released from the TAF1-TFIID complex upon completion of preinitiation complex a

232 tion and transcription; and (3) H3K4me3-TAF3/TFIID interactions regulate gene-selective functions of

233 s, NuA4 plays an important role in targeting TFIID to the promoters of ribosomal protein genes for tr

234 SS selection, in contrast with canonical TBP/TFIID-driven TATA-less promoters that have broader TSS a

235 maining 87% of expressed genes that we term 'TFIID-dependent' are highly sensitive to rapid TFIID dep

236 with the existence of a critical Rap1-TFIIA-TFIID interaction network.

237 d Hmo1), the transcription machinery (TFIIB, TFIID, and RNA polymerase II), and chromatin at near-bas

238 erase II and protein complexes TFIIA, TFIIB, TFIID (or TBP), TFIIE, TFIIF, TFIIH and TFIIK were posit

239 complex (PIC), which contains TFIIA, TFIIB, TFIID, TFIIE, TFIIF, TFIIH, RNAPII, and Mediator.

240 oth TFIID- and SAGA-dependent genes and that TFIID and Mediator occupancy is cooperative.

241 ingle-molecule imaging data demonstrate that TFIID alone binds poorly to native p53 target promoters.

242 the same approach to map TFIID, we find that TFIID is associated with both TFIID- and SAGA-dependent

243 Recent results indicate that TFIID itself is built from distinct preformed submodules

244 Our work indicates that TFIID participates in expression of nearly all yeast mRN

245 This analysis revealed that TFIID coexists in two predominant and distinct structura

246 -molecule dissociation kinetics reveals that TFIID interacts with promoters via transient and prolong

247 mportantly, our structural work reveals that TFIID's conversion to a rearranged DNA binding conformat

248 on, based on recent structural studies, that TFIID may not remain bound to gene promoters through the

249 Despite recent work suggesting that TFIID does not associate with RP genes in Drosophila, we

250 lishing a specific regulatory network at the TFIID-dependent promoter for productive transcriptional

251 nhances the targeting of co-activator at the TFIID-dependent promoter.

252 tational and transcriptional analyses at the TFIID-dependent ribosomal protein genes such as RPS5, RP

253 imentally validated binding site, called the TFIID localization sequence (DLS) and found three times

254 tions in developmental transcription for the TFIID basal transcription factors and for the DNA core p

255 dies have uncovered a novel function for the TFIID subunit TAF7 as a phosphorylation-dependent regula

256 or in vitro, it stably incorporates into the TFIID complex.

257 sequently leads to the disassociation of the TFIID complex and transcription repression.

258 transferase) promotes the recruitment of the TFIID complex for transcriptional initiation.

259 greatly depending on the composition of the TFIID complex in the cell.

260 TAF4b is a subunit of the TFIID complex that is highly expressed in the ovary and

261 TAF7, a component of the TFIID complex that nucleates the assembly of transcripti

262 nt, pausing was lost upon replacement of the TFIID complex with TATA-binding protein (TBP), and PRO-s

263 l to the core promoter and regulators of the TFIID pathway located proximally, and (5) distinct mobil

264 lts of a molecular genetic dissection of the TFIID subunit Taf2.

265 complex in transcriptional activation of the TFIID-dependent genes has not been elucidated.

266 iously shown that Rap1 directly binds to the TFIID complex through interaction with its TATA-binding

267 e SAGA transcription pathway compared to the TFIID pathway, (2) new regulators enriched at tRNA genes

268 nding subunit Tra1 primarily connects to the TFIID-like core via its FAT domain.

269 SAGA complex and CaTAF12 associates with the TFIID complex.

270 CREB showed facilitated interaction with the TFIID subunit coactivator TAF4 assessed by immunoprecipi

271 n (TBP)-associated factors (TAFs) within the TFIID complex and counteracts negative regulators of TBP

272 ter element (DPE) promoter motifs within the TFIID-TFIIA-DNA structure.

273 may function directly or indirectly through TFIID.

274 on how Taf2-Taf14 interaction contributes to TFIID complex organization and identifying a potential r

275 scription is dependent on SAGA as opposed to TFIID.

276 Moreover, TAF6 in flies is restricted to TFIID.

277 se mechanisms and outcomes of transactivator-TFIID interaction remain unclear.

278 e formation of the complex between these two TFIID subunits do not only depend on their histone fold

279 p53 unlocks TFIID's ability to bind DNA by stabilizing TFIID contact

280 nd (5) distinct mobilization of SAGA- versus TFIID-linked regulators during acute heat shock.

281 th the differential occupancy of TAF3 versus TFIID at the MyoD promoter.

282 impairment of tail module function than were TFIID-dependent genes.

283 des evidence that SAGA recruits TBP, whereas TFIID mediates chromatin remodeling.

284 While TFIID subunits and TBP are downregulated during myoblast

285 d DNA sequence that probably associates with TFIID but detected no evidence of RNA secondary structur

286 a molecular switch that interacts first with TFIID in the Pol II initiation complex and then exchange

287 ers and ICP4 has been shown to interact with TFIID, we tested the ability of ICP4 to stabilize the bi

288 d3-10-containing molecules to interact with TFIID.

289 ated in the PIC through its interaction with TFIID but is released from TFIID upon transcription init

290 tivation domain, mediating interactions with TFIID, mediator, and perhaps other transcription factors

291 assays reveal that ERCC1-XPF interacts with TFIID and assembles with POL II and the basal transcript

292 HMGA1 interacts with TFIID and Mediator and is required for the synergy of TA

293 eans by which p53 dynamically interacts with TFIID to facilitate assembly on target gene promoters re

294 TBP, Pol II, and other Mediator modules with TFIID-dependent genes is largely independent of the tail

295 e regulation, its structural similarity with TFIID, and functional interactions between the SAGA modu

296 sruption of the TAF1/TAF7 interaction within TFIID by protein phosphorylation leads to activation of

297 ults uncover distinct contact regions within TFIID bound by each activator.

298 vide evidence that SAGA, not TAF(II)s within TFIID, are largely responsible for TBP recruitment.

299 n whether common or distinct surfaces within TFIID are targeted by activators and what changes if any

300 We have previously shown that yeast TFIID provides coactivator function on the promoters of