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 elongation complexes are less stable than Pol II e

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

4 Pol I mutants lacking either the heterodimeric subunit R

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

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

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

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

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

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

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

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

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 stable than Pol II elongation complexes, and Pol I is more error prone than Pol II.

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

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

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

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

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

23 ription initiation complex including SL1 and Pol I.

24 nscription elongation complex stability, and Pol I pausing in vitro in response to downstream DNA.

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

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

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

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

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

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

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

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

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

34 taneous imaging of all active genes bound by Pol I and the architectural chromatin protein Upstream B

35 The rate of transcription elongation by Pol I directly influences processing of nascent rRNA, an

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

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

38 n transcription initiation and elongation by Pol I.

39 s known roles in transcription elongation by Pol I.

40 ases the rate of transcription elongation by Pol I.

41 ole for Paf1C in transcription elongation by Pol I.

42 s that influence transcription elongation by Pol I.

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

44 t AT-rich downstream DNA enhances pausing by Pol I and inhibits Pol I nucleolytic cleavage activity.

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

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

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

48 itive and negative roles in transcription by Pol I.

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

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

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

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

53 differences between Saccharomyces cerevisiae Pols I and II using a series of quantitative in vitro tr

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

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

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

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

58 43 and A14 in the regulation of differential Pol I complexes assembly and subsequent promoter associa

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

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

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

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

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

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

65 Pol I-specific subunit domains to efficient Pol I passage through nucleosomes in the context of tran

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

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

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

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

70 ES is located within a unique extranucleolar Pol I body called the expression-site body (ESB).

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

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

73 For Pol I, UAF binds to a specific upstream element in the r

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

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

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

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

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

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

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

81 odel for the nucleotide addition pathway for Pol I.

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

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

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

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

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

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

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

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

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

91 ion factor Snai1 (Snail1), RNA Polymerase I (Pol I) and the Upstream Binding Factor (UBF).

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

93 n properties of eukaryotic RNA polymerase I (Pol I) from Saccharomyces cerevisiae has not been define

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

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

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

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

98 RNA polymerase I (Pol I) is a highly efficient enzyme specialized in synth

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

100 NA (rRNA) transcription by RNA polymerase I (Pol I) is the first key step of ribosome biogenesis.

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

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

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

104 Unusually, T. brucei uses RNA polymerase I (Pol I) to transcribe the active ES, which is unprecedent

105 1C and POLR1D) involved in RNA polymerase I (Pol I) transcription account for more than 90% of diseas

106 s dual roles in activating RNA polymerase I (Pol I) transcription and repression of Pol II.

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

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

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

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

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

112 that synthesizes the rRNA, RNA polymerase I (Pol I), and by interactions with cofactors that influenc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 dels suggest that RNA polymerases I and III (Pol I and Pol III) are the only enzymes that directly me

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

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

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

132 s processing of nascent rRNA, and changes in Pol I transcription rate result in alternative rRNA proc

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

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

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

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

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

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

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

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

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

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

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

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

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

146 Increasing Pol I transcription delays differentiation, whereas redu

147 these downstream sequence elements influence Pol I in vivo Native elongating transcript sequencing st

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

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

150 m DNA enhances pausing by Pol I and inhibits Pol I nucleolytic cleavage activity.

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

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

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

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

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

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

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

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

159 ption assays to study purified WT and mutant Pol I variants from the yeast Saccharomyces cerevisiae a

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

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

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

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

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

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

166 n, elongation, and termination activities of Pol I.

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

168 Analysis of Pol I native elongating transcript sequencing data in Sa

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

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

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

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

173 We discuss the contribution of Pol I-specific subunit domains to efficient Pol I passag

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

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

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

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

178 t inhibition involves nucleolar exclusion of Pol I subunits.

179 amage and genomic instability independent of Pol I transcription.

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

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

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

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

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

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

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

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

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

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

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

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

192 ze the nucleotide incorporation mechanism of Pol I.

193 o characterizing the molecular mechanisms of Pol I activity.

194 st insights into the molecular mechanisms of Pol I transcription.

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

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

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

198 odimer could contribute to the regulation of Pol I transcription initiation and elongation.

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

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

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

202 to the sequence entering the active site of Pol I both in vivo and in vitro.

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

204 Cryo-electron microscopy (EM) structures of Pol I initiation and elongation complexes have given fir

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

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

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

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

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

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

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

212 (rDNA) promoter and interacts with two other Pol I initiation factors, the TATA-binding protein (TBP)

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

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

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

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

217 RNA polymerase (Pol) I is a 14-subunit enzyme that solely transcribes pr

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

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

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

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

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

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

224 The shield prevents Pol I from producing sense intergenic noncoding RNAs (si

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

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

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

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

229 Under identical conditions, purified Pol I and Pol III, but not Pol II, could transcribe nucl

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

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

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

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

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

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

236 cription, but overlap in function during RNA Pol I-mediated gene expression during host immune evasio

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

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

239 2-subunit phosphorylated and inactivated RNA Pol I (polymerase I)-associated transcription factor TIF

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

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

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

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

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

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

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

247 and DNA damage accumulation in telomeric RNA Pol I transcription sites, also leading to altered gene

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

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

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

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

252 Since Pol I transcribes rDNA repeats with high processivity an

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

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

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

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

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

258 We find that Pol I single-nucleotide and multinucleotide addition rat

259 ng transcript sequencing studies reveal that Pol I occupancy increases as downstream AT content incre

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

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

262 It has been suggested that Pol I-associated factors facilitate chromatin transcript

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

264 III promoters, and very slow turnover at the Pol I promoter.

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

266 ht into the functional interplay between the Pol I-specific transcription-like factors A49-A34.5 and

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

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

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

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

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

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

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

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

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

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

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

278 ition at each round of rDNA replication, the Pol I transcription machinery has to deal with nucleosom

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

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

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

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

287 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

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

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

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

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

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

293 ontain 1 subnuclear ESB, as determined using Pol I or the ESB marker VEX1.

294 tin transcription, but it is unknown whether Pol I has an intrinsic capacity to transcribe through nu

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

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

297 nucleolus, and enhances its interaction with Pol I.

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

299 Here, we present cryo-EM structures of yeast Pol I elongation complexes (ECs) bound to the nucleotide

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