ライフサイエンスコーパス: Pol I

1 Pol I activity is commonly deregulated in human cancers.

2 Pol I is protected by its subunit A12.2, which decreases

3 Pol I occupancy of the coding region of the rDNA in THO

4 Pol I transcription in hpr1 or tho2 null mutants is dram

5 Pol I's mutational footprint suggests: (i) during leadin

6 The active VSG gene is in a Pol I-transcribed telomeric expression site (ES).

7 This demonstrates the essentiality of a Pol I-transcribed ES, as well as conserved VSG 3'UTR 16-

8 tivation of upstream binding factor (UBF), a Pol I DNA binding transcription factor.

9 First, Spt6 physically associates with a Pol I subunit (Rpa43).

10 th the eukaryotic RNAP subunits A43 and A14 (Pol I), Rpb7 and Rpb4 (Pol II), and C25 and C17 (Pol III

11 tream activation factor, is known to abolish Pol I transcription and derepress Pol II transcription o

12 monstrate that human SL1 can direct accurate Pol I transcription in the absence of UBF and can intera

13 Binding of initiation factor Rrn3 activates Pol I, fostering recruitment to ribosomal DNA promoters.

14 Changes in Maf1 expression affect Pol I- and Pol III-dependent transcription in human glio

15 etically with Spt4/5, which directly affects Pol I transcription.

16 ructurally and functionally homologous among Pols I through V are assigned equivalent numbers.

17 We conclude that Fob1 and Pol I make independent contributions to establishment of

18 l RNA synthesis rates, rDNA copy number, and Pol I occupancy of the rDNA demonstrate that Spt5p plays

19 tic interactions between genes for Paf1C and Pol I subunits confirm this conclusion.

20 f typical rDNA silencing, including RENT and Pol I dependence, as well as a requirement for the Preis

21 n, however, which involves the silencing and Pol I-mediated transcriptional switching of subtelomeric

22 o the promoter-specific targeting of SL1 and Pol I during PIC assembly.

23 ription initiation complex including SL1 and Pol I.

24 nidentified tight binding states for Taq and Pol I (KF) DNA polymerases.

25 it RNA polymerases I and III (abbreviated as Pol I and Pol III), the first analysis of their physical

26 multisubunit RNA polymerases, abbreviated as Pol I, Pol II and Pol III.

27 uclear RNA polymerases (Pols) referred to as Pols I, II, and III, each of which synthesizes a specifi

28 cle stages and show similar distributions at Pol I-transcribed loci.

29 Distribution of TDP1 at Pol I-transcribed loci is inversely correlated with hist

30 Thus, the RNA output by both Pol I and II is reduced in Chd1(-/-) cells.

31 centrations that provide information on both Pol I's nucleotide addition and nuclease activities.

32 wild-type cells and produce rRNA using both Pol I and Pol II.

33 mportant role in transcription elongation by Pol I in vivo.

34 s transcription initiation and elongation by Pol I, identifying a new cellular target for the conserv

35 s known roles in transcription elongation by Pol I.

36 ases the rate of transcription elongation by Pol I.

37 ole for Paf1C in transcription elongation by Pol I.

38 s that influence transcription elongation by Pol I.

39 n transcription initiation and elongation by Pol I.

40 iation and elongation, at promoter escape by Pol I.

41 ce transcription of the active rRNA genes by Pol I and of Pol III-transcribed genes.

42 oaches to characterize the role(s) played by Pol I in the dnaN159 strain.

43 RNA genes, which are normally transcribed by Pol I and Pol III.

44 buted to the increased rDNA transcription by Pol I in cancer.

45 itive and negative roles in transcription by Pol I.

46 d on the initiation step of transcription by Pol I; however, recent studies in yeast and mammals have

47 Transcription by Pols I and III is restrained in healthy cells by the tum

48 majority of transcription in growing cells, Pol I regulation is poorly understood compared to Pol II

49 olve a structure of Saccharomyces cerevisiae Pol I-CF-DNA to 3.8 A resolution using single-particle c

50 BP]G*), is processed in a well-characterized Pol I family model replicative DNA polymerase, Bacillus

51 hese results suggest that (i) the beta clamp-Pol I interaction may be important for proper Pol I func

52 for the 5'-3' exonuclease Rat1 that degrades Pol I-associated transcripts destabilizing the transcrip

53 O(6)-(benzotriazol-1-yl)inosine derivatives (Pol-I and Pol-dI) have been synthesized reasonably effec

54 43 and A14 in the regulation of differential Pol I complexes assembly and subsequent promoter associa

55 new model for how TCS mutations may disrupt Pol I and III complex integrity.

56 ups, but the primosomal protein PriA and DNA Pol I contributed.

57 the Klenow fragment of Escherichia coli DNA Pol I (exo-) in single-nucleotide insertions.

58 Klenow fragment (Kf) of Escherichia coli DNA Pol I.

59 Kinetics studies with DNA Pol I (Klenow fragment, exonuclease-deficient) in vitro

60 X1, the exonuclease domains from E. coli DNA-Pol I, and the DNA polymerase of bacteriophage RB69.

61 This suggests that dysregulated Pol I transcription is essential for the maintenance of

62 of Pol I subunits or insertion of an ectopic Pol I terminator within the adjacent rDNA gene.

63 onstrate that protein levels of an essential Pol I initiation factor, Rrn3, are reduced when Spt6 is

64 ved that Spt5 directly binds to an essential Pol I transcription initiation factor, Rrn3, and to the

65 nes, POLR1C and POLR1D, encode for essential Pol I/III subunits that form a heterodimer necessary for

66 nderscoring the parallels between eukaryotic Pol I, II, and III and archaeal transcription machinerie

67 bility group box (HMGB) protein facilitating Pol I transcription in T. brucei.

68 architectural chromatin protein facilitating Pol I-mediated transcription of both protein coding gene

69 transcription factors have been defined for Pol I in mammals, the selectivity factor SL1, and the up

70 pt6-1004, we show that Spt6 is essential for Pol I occupancy of the ribosomal DNA (rDNA) and rRNA syn

71 SL1, essential for Pol I recruitment to the ribosomal RNA gene promoter, al

72 nally related to parts of these factors (for Pol I and Pol III).

73 ffected, implying that FACT is important for Pol I transcription elongation through chromatin.

74 o studies revealed a 'torpedo' mechanism for Pol I termination: co-transcriptional RNA cleavage by Rn

75 bunits that form a heterodimer necessary for Pol I/III assembly, and many TCS mutations lie along the

76 odel for the nucleotide addition pathway for Pol I.

77 general reductions in new transcription from Pol I, II, and III genes.

78 earing the dnaN159 allele require functional Pol I for viability.

79 Furthermore, Pol I and Pol II use distinct mechanisms to avoid nonrec

80 nscription units, providing insight into how Pol I transcription is controlled.

81 We report that TAF1B, a subunit of human Pol I basal transcription factor SL1, is structurally re

82 des with the repression of RNA polymerase I (Pol I) activity.

83 leads to an inhibition of RNA Polymerase I (Pol I) activity.

84 transcriptional control by RNA polymerase I (Pol I) and associated factors is well studied, the linea

85 Notably, RNA polymerase I (Pol I) and Pol II recover from shallow backtracks by 1D

86 ), where it interacts with RNA polymerase I (Pol I) as well as with histones.

87 ranscription initiation by RNA Polymerase I (Pol I) depends on the Core Factor (CF) complex to recogn

88 a role in transcription by RNA polymerase I (Pol I) in Saccharomyces cerevisiae.

89 ntial for transcription by RNA polymerase I (Pol I) in the parasite Trypanosoma brucei.

90 y of Cdc14 is required for RNA polymerase I (Pol I) inhibition in vitro and in vivo.

91 RNA polymerase I (Pol I) is a dedicated polymerase that transcribes the 45

92 , transcription of rRNA by RNA polymerase I (Pol I) is an important target for the regulation of this

93 RNA gene transcription by RNA polymerase I (Pol I) is the driving force behind ribosome biogenesis,

94 , we identify a Drosophila RNA polymerase I (Pol I) regulatory complex composed of Under-developed (U

95 s transcribed from rDNA by RNA polymerase I (Pol I) to produce the 45S precursor of the 28S, 5.8S, an

96 NA) synthesis by tethering RNA polymerase I (Pol I) to the rDNA promoter.

97 1C and POLR1D) involved in RNA polymerase I (Pol I) transcription account for more than 90% of diseas

98 Regulation of RNA polymerase I (Pol I) transcription is critical for controlling ribosom

99 n that associates with the RNA polymerase I (Pol I) transcription machinery to suppress rRNA gene tra

100 inability to fully reactivate polymerase I (Pol I) transcription when cells exit stationary phase.

101 the selective inhibitor of RNA polymerase I (Pol I) transcription, CX-5461, effectively treats aggres

102 topic, there is codominance in polymerase I (Pol I) transcription.

103 ntly and rapidly represses RNA polymerase I (Pol I) transcription.

104 through interactions with RNA polymerase I (Pol I), and to a pair of DNA replication fork block site

105 that family, Escherichia coli polymerase I (Pol I), may also be able to bypass these large major gro

106 ranscription, catalyzed by RNA polymerase I (Pol I), plays a critical role in ribosome biogenesis, an

107 rated the critical role of RNA polymerase I (Pol I)-associated factor PAF53 in mammalian rRNA transcr

108 -box helicases involved in RNA polymerase I (Pol I)-mediated transcriptional activity.

109 to function exclusively in RNA polymerase I (Pol I)-specific transcription of the ribosomal genes.

110 ess, TbISWI down-regulates RNA polymerase I (Pol I)-transcribed variant surface glycoprotein (VSG) ge

111 monoallelic fashion using RNA polymerase I (Pol I).

112 osomal DNA (rDNA) genes by RNA polymerase I (Pol I).

113 ng blocks of ribosomes) by RNA Polymerase I (Pol I).

114 thesis of ribosomal RNA by RNA polymerase I (Pol I).

115 NA (rDNA) transcription by RNA polymerase I (Pol I).

116 egulating transcription by RNA polymerase I (Pol I).

117 y affects transcription by RNA polymerase I (Pol I).

118 Transcription by RNA polymerase I (Pol-I) is the main driving force behind ribosome biogene

119 Our results identify Pol I transcription-dependent processes as a novel means

120 al in combination with mutations that impair Pol I transcription initiation and elongation.

121 Changes in Pol I transcription at this gene alter the expression of

122 role in ribosome biogenesis, and changes in Pol I transcription rate are associated with profound al

123 evious studies only characterized defects in Pol I transcription induced by deletion of SPT4.

124 bly and postpolymerase recruitment events in Pol I transcription, underscoring the parallels between

125 xpectedly, UBTF2, which does not function in Pol I transcription, is sufficient to regulate histone g

126 SL1, TAF(I)41 (MGC5306), which functions in Pol I transcription.

127 showed a small but reproducible increase in Pol I density in a region near the 5' end of the gene.

128 Increases in Pol I transcription induce growth on media containing 5-

129 Consistent with a direct role for Mot1 in Pol I transcription, Mot1 also associates with the Pol I

130 ter cassette (mURA3) such that reductions in Pol I transcription induce growth on synthetic media lac

131 nclude that SWI/SNF plays a positive role in Pol I transcription, potentially by modifying chromatin

132 To examine their functional role in Pol I transcription, we constructed yeast strains in whi

133 y function of yeast core factor/human SL1 in Pol I transcription.

134 for SL1, including the TAF(I)41 subunit, in Pol I recruitment and, therefore, preinitiation complex

135 plexes, followed by the assembly of inactive Pol I homodimers.

136 Increased Pol-I transcription and the concurrent increase in ribos

137 Overexpression of SIRT7 increases Pol I-mediated transcription, whereas knockdown of SIRT7

138 Increasing Pol I transcription delays differentiation, whereas redu

139 budding yeast, like most eukaryotes, inhibit Pol I transcription before segregation as a prerequisite

140 mplexes in the nucleolus, thereby inhibiting Pol I transcription and inducing apoptosis in cancer cel

141 CX-5461 selectively inhibits Pol I-driven transcription relative to Pol II-driven tra

142 t AC40 paralogs, one of which assembles into Pol I and the other of which assembles into Pol III.

143 Most previous investigations into Pol I transcription regulation have focused on transcrip

144 such that it is no longer impacted by local Pol I transcription defects.

145 leftmost rDNA gene to investigate localized Pol I and Fob1 functions in silencing.

146 rify and co-immunoprecipitate with mammalian Pol I complexes.

147 ctron cryomicroscopy structures of monomeric Pol I alone and in complex with Rrn3, underscores the ce

148 Moreover, Pol I dimers also form after inhibition of either riboso

149 clear DNA-dependent RNA polymerases, namely, Pol I, II, and III.

150 zation of either Rrn7 N-terminal domain near Pol I wall or the tandem winged helix domain of A49 at a

151 with RNA polymerase II (Pol II), but neither Pol I- nor Pol III-transcribed regions in the budding ye

152 posure of the polymer-supported nucleosides, Pol-I and Pol-dI, to alcohol, phenol, thiol and amine nu

153 n) resulted in a strong inhibition (>80%) of Pol I transcription.

154 Far Western blot analysis implicates A190 of Pol I as well as Rpb1 of Pol II in binding Spt5.

155 function in vivo and (ii) in the absence of Pol I, ssDNA gaps may persist in the dnaN159 strain, lea

156 properties required for potent activation of Pol I stress and cytotoxicity.

157 The key activator of Pol I transcription, UBF, has been proposed to act by fa

158 s work reports the most detailed analysis of Pol I mechanism to date.

159 activity results in decreased association of Pol I with rDNA and a reduction of Pol I transcription.

160 DHX33 knockdown decreased the association of Pol I with rDNA and caused a dramatic decrease in levels

161 nce that coilin modulates the association of Pol I with ribosomal DNA.

162 nd ChIP experiments show that association of Pol I with the rRNA gene is reduced in RPS19-depleted ce

163 deprivation, cells induce rapid clearance of Pol I-Rrn3 complexes, followed by the assembly of inacti

164 date, the factors involved in the control of Pol I transcription elongation are poorly understood.

165 unction is required for efficient control of Pol I transcription in response to target of rapamycin (

166 atives that contribute to the development of Pol I inhibitory cancer therapeutic strategies.

167 correlate with the functional divergence of Pol I- and Pol III-specific AC40 paralogs.

168 icient rRNA transcription, or elimination of Pol I activity, which drives rRNA transcription, diminis

169 t inhibition involves nucleolar exclusion of Pol I subunits.

170 amage and genomic instability independent of Pol I transcription.

171 e degraded by proteasomes upon inhibition of Pol I activity by actinomycin D, L5 and L11 accumulate i

172 ent apoptotic cell death), the inhibition of Pol I transcription also demonstrates potent efficacy in

173 that Rpd3 is not required for inhibition of Pol I transcription by rapamycin, supporting the model t

174 Most strikingly, the acute inhibition of Pol I transcription reduces both the leukemic granulocyt

175 xamides have been evaluated as inhibitors of Pol I and activators of the destruction of RPA194, the P

176 Thus, selective inhibitors of Pol I may offer a general therapeutic strategy to block

177 n of SL1 to the extracts raises the level of Pol I transcription.

178 ur findings indicate that elevated levels of Pol I partially suppress the temperature-sensitive growt

179 s from these cells support reduced levels of Pol I transcription; addition of SL1 to the extracts rai

180 pt6 is inactivated, leading to low levels of Pol I-Rrn3 complex.

181 Global loss of Pol I activity, however, negatively affects Fob1 associa

182 A promoter in vivo, with concomitant loss of Pol I from the rDNA and reduced synthesis of the pre-rRN

183 Silencing was attenuated by loss of Pol I subunits or insertion of an ectopic Pol I terminat

184 ze the nucleotide incorporation mechanism of Pol I.

185 o characterizing the molecular mechanisms of Pol I activity.

186 such as c-Myc, that stimulate the output of Pol I and Pol III.

187 he beta clamp stimulates the processivity of Pol I in vitro and that beta159 is impaired for this act

188 A194, the large catalytic subunit protein of Pol I holocomplex, and this correlates with cancer cell

189 oposed to act by facilitating recruitment of Pol I and essential basal factor SL1 to rDNA promoters.

190 iation of Pol I with rDNA and a reduction of Pol I transcription.

191 teract with RPA-194 and the key regulator of Pol I activity, upstream binding factor (UBF).

192 uggest that SIRT7 is a positive regulator of Pol I transcription and is required for cell viability i

193 Spt5p, and, potentially, other regulators of Pol I transcription elongation play important roles in c

194 phosphorylation of three known regulators of Pol I, CDK2, AKT and AMPK, is altered during ribosomal s

195 er is necessary to direct multiple rounds of Pol I transcription initiation.

196 s important for promoting multiple rounds of Pol I transcription.

197 eukaryotic cells, including the silencing of Pol I and Pol II transcribed genes, silencing of replica

198 fy distinct backtrack recovery strategies of Pol I and Pol II, shedding light on the evolution of cel

199 coilin with RPA-194 (the largest subunit of Pol I), and we further show that coilin can specifically

200 Three additional subunits of Pol I may also participate in this interaction.

201 Their study reveals that three subunits of Pol I perform functions in transcription elongation that

202 vivo is fundamentally different from that of Pol I and whether the static behavior of Pol II factors

203 icine, are potent and specific inhibitors of Pol-I transcription, with IC(50) in vitro and in cells i

204 rains to characterize the effect of Spt5p on Pol I transcription.

205 ignificant alteration of rDNA copy number or Pol I occupancy of the rDNA.

206 of UBF, Ser388 phosphorylated UBF, and other Pol I-related components (POLR1E, TAF1A, and TAF1C) rema

207 ntroduce a new nomenclature system for plant Pol I and Pol III subunits in which the 12 subunits that

208 anscriptional status of both RNA polymerase (Pol) I and II to control multiple steps of ribosome biog

209 Transcription by RNA polymerase (Pol) I and III was induced by EGF.

210 pt5 directly associates with RNA polymerase (Pol) I and RNA Pol II in yeast through its central regio

211 ture of the 14-subunit yeast RNA polymerase (Pol) I enzyme at 12 A resolution using cryo-electron mic

212 the mechanisms that control RNA Polymerase (Pol) I transcription have primarily focused on the proce

213 itiation factor required for RNA polymerase (Pol) I transcription in Saccharomyces cerevisiae, contai

214 ibosomal RNA, transcribed by RNA polymerase (Pol) I, accounts for most cellular RNA.

215 RNA polymerase (Pol) I, the multiprotein complex that synthesizes rRNA,

216 ynthesis of ribosomal RNA by RNA polymerase (Pol) I; however, previous studies only characterized def

217 e first time that the major DNA polymerases (Pol I and Pol III) and DNA ligase are directly involved

218 anslational modification of RNA polymerases (Pol) I and II by acetylation mediates the transcriptiona

219 RNA), which are produced by RNA polymerases (Pols) I and III.

220 her, these data indicate that Paf1C promotes Pol I transcription through the rDNA by increasing the n

221 ol I interaction may be important for proper Pol I function in vivo and (ii) in the absence of Pol I,

222 onal RNA cleavage event at T1 which provides Pol I with an alternative termination pathway.

223 -kinase) and two other family members [PTRF (Pol I and transcription release factor) and SDPR] functi

224 Inhibition of CK2 kinase activity reduces Pol I transcription in cultured cells and in vitro.

225 n from nuclear extracts dramatically reduces Pol I transcription; addition of SL1 restores the abilit

226 products of proto-oncogenes can up-regulate Pol I, whereas tumor suppressor proteins can inhibit rRN

227 he rRNA gene promoter and directly regulates Pol I transcription re-initiation by stabilizing the ass

228 entral transcription factor, which regulates Pol I, Pol II and Pol III gene activity.

229 our data suggest that coilin acts to repress Pol I activity in response to cisplatin-induced DNA dama

230 Overexpression of RRN3 rescues Pol I-Rrn3 complex formation; however, rRNA synthesis is

231 RNA Pol I is regulated through PI3 kinase/Akt/mammalian targ

232 tionally, the nucleolus disassembled and RNA Pol I activity declined after RNA Pol II inhibition.

233 CITFA2 resulted in a loss of CITFA from RNA Pol I promoters.

234 etween the dynamics of RNA polymerase I (RNA Pol I) assembly and transcriptional output.

235 of the large rRNAs by RNA polymerase I (RNA Pol I) was investigated.

236 2-subunit phosphorylated and inactivated RNA Pol I (polymerase I)-associated transcription factor TIF

237 nucleolar proteome but does not inhibit RNA Pol I transcription.

238 nal arrest as evidenced by inactivity of RNA Pol I and II and the subsequent alteration in nuclear su

239 is accompanied by prolonged retention of RNA Pol I components at the promoter, resulting in longer pr

240 Pol II, but also acts as a repressor of RNA Pol I mediated rRNA synthesis.

241 n between expression, hypomethylation of RNA Pol I promoters and chromatin decondensation was apparen

242 edly with the highly dynamic behavior of RNA Pol I transcription complexes in vivo, which undergo cyc

243 tion factor and that T. brucei relies on RNA Pol I for expressing the variant surface glycoprotein (V

244 results demonstrate that PTEN represses RNA Pol I transcription through a novel mechanism that invol

245 f PTEN in PTEN-deficient cells represses RNA Pol I transcription, while decreasing PTEN expression en

246 ur biochemical analyses demonstrate that RNA Pol I can transcribe through nucleosome templates and th

247 No change in the expression of the RNA Pol I transcription components, upstream binding factor

248 ith open chromatin, co-localize with the RNA Pol I transcription factor UBF1, and undergo transition

249 (rDNA) loci, where it interacts with the RNA Pol I transcription factor upstream binding factor (UBF)

250 Runx2 forms complexes containing the RNA Pol I transcription factors UBF1 and SL1, co-occupies th

251 Since Pol I transcribes rDNA repeats with high processivity an

252 te that despite its constrained active site, Pol I can catalyze DNA synthesis past N(6)-dA-linked pep

253 The reduced ability of beta159 to stimulate Pol I in vitro correlates with our finding that single-s

254 ead to deregulated signaling that stimulates Pol I transcription with resultant increases in ribosome

255 res the ability of these extracts to support Pol I transcription.

256 ng de novo DNA methylation fails to suppress Pol I or Pol II transcription in the absence of HDA6 act

257 Our results show that Pol I activity is under proteasome-mediated control, whi

258 The results showed that Pol I and Pol II could efficiently and accurately bypass

259 We have shown that Pol-I inhibition occurs by a p53-, ATM/ATR-, and Top2-in

260 protein, RNA polymerase II (Pol II), and the Pol I-associated transcription factor SL1 could be preci

261 ere is a biochemical interaction between the Pol I-associated heterodimer and Rrn3 and that this inte

262 eous levels of VSG117 were obtained from the Pol I-transcribed rDNA.

263 vidence that HDV RNA synthesis occurs in the Pol I and Pol II transcription machineries, thus extendi

264 A TFIIB-like protein was not evident in the Pol I basal transcription machinery.

265 a strain, which lacks the A49 subunit in the Pol I complex.

266 with different conformational states of the Pol I cleft, in addition to the stabilization of either

267 enow and Klentaq, the large fragments of the Pol I DNA polymerases from Escherichia coli and Thermus

268 However, none of the Pol I factors were known to share homology with transcri

269 a reaction that depends on components of the Pol I general transcription machinery.

270 ggesting a less-efficient recruitment of the Pol I machinery from the RDN1 locus.

271 ession and for inhibiting recruitment of the Pol I machinery to the rDNA promoter.

272 sing intermediates or the recruitment of the Pol I transcription factor UBTF.

273 of RRN9 encoding an essential subunit of the Pol I transcription factor, upstream activation factor,

274 n contrast to related DNA polymerases of the Pol I type, which fail to extend mismatches efficiently

275 of endogenous coilin partially overrides the Pol I transcriptional arrest caused by cisplatin, while

276 at Spt6 is involved in either recruiting the Pol I-Rrn3 complex to the rDNA or stabilizing the preini

277 activators of the destruction of RPA194, the Pol I large catalytic subunit protein.

278 RNA synthesis through direct binding to the Pol I complex.

279 ociation of HDV replication complex with the Pol I and Pol II transcription machineries.

280 in kinase CK2 co-immunoprecipitates with the Pol I complex and is associated with the rRNA gene promo

281 FLNA coimmunoprecipitated with the Pol I components actin, TIF-IA, and RPA40, and their occ

282 transcription, Mot1 also associates with the Pol I promoter in vitro in a reaction that depends on co

283 increase in histones H3, H2A and H1 at these Pol I transcription units.

284 utions to establishment of silencing, though Pol I also reinforces Fob1-dependent silencing.

285 ed by RNA polymerase (Pol) II in addition to Pol I, but Pol II transcription is usually silenced.

286 me analysis suggests specific alterations to Pol I-dependent transcription.

287 However, hypoacetylated heterodimer binds to Pol I with greater affinity than acetylated heterodimer.

288 o date, AC40 and AC19 subunits are common to Pol I (a.k.a. Pol A) and Pol III (a.k.a. Pol C) and are

289 ic recruitment of CE to Pol II as opposed to Pol I and Pol III rests on the interaction between CE an

290 in CE interaction with Pol II as opposed to Pol I and Pol III.

291 As the binding of Rrn3 to Pol I is essential to transcription initiation in yeast

292 onship with histones on actively transcribed Pol I transcription units, providing insight into how Po

293 inating the expression of highly transcribed Pol I (UBTF1 activity) and Pol II genes (UBTF2 activity)

294 emonstrate that DDX21 widely associates with Pol I- and Pol II-transcribed genes and with diverse spe

295 found that these two proteins copurify with Pol I and associate with the rDNA in vivo.

296 e rDNA repeat and interacts genetically with Pol I transcription initiation factors.

297 nucleolus, and enhances its interaction with Pol I.

298 at Pol IV does not functionally overlap with Pol I, II, or III and is nonessential for viability.

299 und that the association of PAF49/PAF53 with Pol I is regulated.

300 re we show that Rrn7, a subunit of the yeast Pol I core factor, and its human ortholog TAF1B are TFII