ライフサイエンスコーパス: Pol II

1 Pol II elongation rates of 2.4-3.0 kb/min were observed,

2 Genetic ablation of Cobra1, which encodes a Pol II-pausing and BRCA1-binding protein, ameliorates R-

3 ith the synthesis of one RNA molecule across Pol II genes, suggesting multiple rounds of pre-initiati

4 ationalize how chromatin arrangement affects Pol II transcription dynamics.

5 its "OFF"/"ON" time ratios but did not alter Pol II firing rates during the "ON" period.

6 f transcription defects derived from altered Pol II activity mutants, essential for their use as prob

7 Finally, we tested a model that altered Pol II activity sensitizes cells to nucleotide depletion

8 o facilitate "on-site" P-TEFb activation and Pol II elongation.

9 t Pols IV and V differ from one another, and Pol II, in nucleotide incorporation rate, transcriptiona

10 and functional similarities between Bdp1 and Pol II factors TFIIA and TFIIF, and unravels essential i

11 Based on CAGE and Pol II localization data, we found strong evidence of tr

12 mRNA counts, Pol II density and Pol II firing rates of the Ccnb1 promoter transgene rese

13 regulate stage-specific gene expression and Pol II pausing will contribute to our continuous search

14 subsets of general transcription factors and Pol II can form stable complexes that are precursors for

15 Furthermore, Pol I and Pol II use distinct mechanisms to avoid nonrecoverable b

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

17 suggesting that transcription initiation and Pol II release are the key determinants of gene control

18 5-P) CTD-specific splicing intermediates and Pol II accumulation over co-transcriptionally spliced ex

19 omplex including GATA1, TAL1, LMO2, LDB1 and Pol II at least, in erythroid cells.

20 Notably, the interaction of p53 and Pol II leads to increased Pol II elongation activity.

21 oximal pausing, while Pol II recruitment and Pol II pausing are not correlated among non-NL genes.

22 n through cyclin T1 and Cdk9 recruitment and Pol II Ser2 phosphorylation.

23 ors results in defective NNS termination and Pol II readthrough.

24 at associates with RNA polymerases Pol V and Pol II, and is required for RNA-directed DNA methylation

25 de occurs by reduced binding of RARalpha and Pol-II at the Fgf21 promoter.

26 teins to be recruited to the lesion-arrested Pol II during the initiation of eukaryotic TCR.

27 How cells distinguish DNA lesion-arrested Pol II from other forms of arrested Pol II, the role of

28 arrested Pol II from other forms of arrested Pol II, the role of CSB in TCR initiation, and how CSB i

29 ion, and how CSB interacts with the arrested Pol II complex are all unknown.

30 transcript release from chromatin-associated Pol II.

31 Understanding the time lag between Pol II progression and splicing could provide mechanisti

32 uman Mediator head module subunits that bind Pol II independent of other subunits and thus probably c

33 found that Mediator, in addition to binding Pol II promoters, occupies chromosomal interacting domai

34 This study reveals that p53 binds Pol II via the Rpb1 and Rpb2 subunits, bridging the DNA-

35 cy of NNS termination by physically blocking Pol II progression.

36 Thus, CBP directly stimulates both Pol II recruitment and the ability to traverse the first

37 n2, required in transcription termination by Pol II, which we validated as a bona fide P-TEFb substra

38 we report the structure of the S. cerevisiae Pol II-Rad26 complex solved by cryo-electron microscopy.

39 m CARE, Atf4, C/ebp-homology protein (Chop), Pol II and TATA-binding protein exhibited enhanced recru

40 II poising in B cell activation, we compared Pol II profiles in resting and activated B cells.

41 on small RNA regulatory circuits containing Pol II transcribed microRNAs (miRNAs).

42 In contrast, Pol II is fully protected through association with the c

43 mRNA counts, Pol II density and Pol II firing rates of the Ccnb1 prom

44 e the consequences of increased or decreased Pol II catalysis on gene expression in Saccharomyces cer

45 ate, either fast or slow, leads to decreased Pol II occupancy and apparent reduction in elongation ra

46 t in this case, Runt prevents PESE-dependent Pol II recruitment and preinitiation complex (PIC) assem

47 ly, mNET-seq patterns specific for different Pol II CTD phosphorylation states reveal weak co-transcr

48 rength, altered TSS selection and diminished Pol II recruitment.

49 (Pol II) recruitment levels tend to display Pol II promoter-proximal pausing, while Pol II recruitme

50 Disrupting Pol II pausing machinery causes a severe reduction of HS

51 ese roadblocks, demonstrating that effective Pol II termination depends on a synergy between the NNS

52 Furthermore, inactivating NNS enables Pol II elongation through these roadblocks, demonstratin

53 in the living cells, we captured endogenous Pol II clusters.

54 I coupled with the degradation of endogenous Pol II using a toxin, alpha-amanitin.

55 Here we label the endogenous Pol II in mouse embryonic fibroblast (MEF) cells using t

56 s economy of design enables Rtt103 to engage Pol II at distinct sets of genes with differentially enr

57 inds to the CTD of transcriptionally engaged Pol II.

58 oteins leads to strong depletion of enhancer Pol II occupancy and eRNA synthesis, concomitant with do

59 onsistent with this finding, loci exhibiting Pol II readthrough at GRF binding sites are depleted for

60 with previous observations in the exogenous Pol II MEF cell line.

61 chromatin opening) and that GAF-facilitated Pol II pausing is critical for HS activation.

62 tly of mRNA-capping activity in facilitating Pol II's engagement in transcriptional elongation, thus

63 genetic networks, each containing just a few Pol II transcribed genes, that generate specific signal-

64 First, Pol II elongation complexes are isolated with specific p

65 dle module and markedly reduced affinity for Pol II.

66 Some promoters have a strong disposition for Pol II pausing and often mediate faster, more synchronou

67 phila melanogaster CTD that is essential for Pol II function in vivo and capitalize on natural sequen

68 results suggested that RDM4 is important for Pol II occupancy at the promoters of CBF2 and CBF3.

69 restingly, CBP activity is rate limiting for Pol II recruitment to these highly paused promoters thro

70 ced products observed as introns emerge from Pol II.

71 x on transcribed genes when RNA emerges from Pol II, and that loss of EF-RNA interactions upon RNA cl

72 F-E results in the dissociation of NELF from Pol II, thereby transiting transcription from pausing to

73 However, it is still unknown how Pol II pausing is regulated by Cet1.

74 bunit RNA polymerases, abbreviated as Pol I, Pol II and Pol III.

75 Here we employ a set of RNA Polymerase II (Pol II) activity mutants to determine the consequences o

76 ssed by the inhibition of RNA polymerase II (Pol II) activity.

77 t stable interactions between polymerase II (Pol II) and a heteroduplex DNA template do not depend on

78 ryotes are transcribed by RNA polymerase II (Pol II) and introns are removed from pre-mRNA by the spl

79 During mitosis, RNA polymerase II (Pol II) and many transcription factors dissociate from c

80 mplex (PIC) that includes RNA polymerase II (Pol II) and the general transcription factors TFIID, TFI

81 nstitutive association of RNA polymerase II (Pol II) and the general transcription machinery near the

82 The dynamics of the RNA polymerase II (Pol II) backtracking process is poorly understood.

83 H-kinase Kin28/Cdk7 marks RNA polymerase II (Pol II) by phosphorylating the C-terminal domain (CTD) o

84 Phosphorylation of the RNA polymerase II (Pol II) C-terminal domain (CTD) regulates transcription

85 ation factor PCF11 on its RNA polymerase II (Pol II) C-terminal domain (CTD)-interacting domain (CID)

86 hesis and the dynamics of RNA Polymerase II (Pol II) clusters at a gene locus.

87 of Rpb1, a subunit of the RNA polymerase II (Pol II) complex, and therefore hampers global cellular t

88 he transcription cycle of RNA polymerase II (Pol II) correlates with changes to the phosphorylation s

89 al inhibitor studies that RNA polymerase II (Pol II) elongation is important for establishing memory

90 romoter-proximally paused RNA polymerase II (Pol II) formation (likely at the step of chromatin openi

91 cell imaging of mammalian RNA polymerase II (Pol II) has previously relied on random insertions of ex

92 itation of histone H3 and RNA polymerase II (Pol II) in mutants lacking single or multiple cofactors

93 e P-TEFb to phosphorylate RNA polymerase II (Pol II) in response to stimuli.

94 l accumulation/pausing of RNA polymerase II (Pol II) independently of its capping activity in Sacchar

95 moter-proximal pausing by RNA polymerase II (Pol II) is a key rate-limiting step in HIV-1 transcripti

96 Transcription by RNA polymerase II (Pol II) is dictated in part by core promoter elements, w

97 he transcription cycle of RNA polymerase II (Pol II) is regulated at discrete transition points by cy

98 Transcription by RNA polymerase II (Pol II) is required to produce mRNAs and some noncoding

99 F and NELF with initiated RNA Polymerase II (Pol II) is the general mechanism for inducing promoter-p

100 Elongation of RNA polymerase II (Pol II) is thought to be an important mechanism for regu

101 d characterization of the RNA polymerase II (Pol II) kinase Cdk12 as a factor that is required for Nr

102 minal domain (CTD) of the RNA polymerase II (Pol II) large subunit cycles through phosphorylation sta

103 ers to study single yeast RNA polymerase II (Pol II) molecules transcribing along a DNA template with

104 unexpectedly showed that RNA polymerase II (Pol II) occupancy changes at FLC did not reflect RNA fol

105 occurs in the absence of RNA polymerase II (Pol II) occupancy, transcription, and replication.

106 of the largest subunit of RNA polymerase II (Pol II) orchestrates dynamic recruitment of specific cel

107 RNA polymerase II (Pol II) pauses downstream of the transcription initiatio

108 es with promoter-proximal RNA polymerase II (Pol II) pausing.

109 ent and the regulation of RNA polymerase II (Pol II) pausing.

110 moter-proximal pausing of RNA polymerase II (Pol II) plays a critical role in regulating metazoan gen

111 Brd4 temporally controls RNA polymerase II (Pol II) processivity during transcription elongation thr

112 metazoans is regulated by RNA polymerase II (Pol II) promoter-proximal pausing and its release.

113 ption activation involves RNA polymerase II (Pol II) recruitment and release from the promoter into p

114 tive NL genes with higher RNA polymerase II (Pol II) recruitment levels tend to display Pol II promot

115 at many steps, including RNA polymerase II (Pol II) recruitment, transcription initiation, promoter-

116 RNA Polymerase II (Pol II) regulatory cascades involving transcription fact

117 The RNA polymerase II (Pol II) transcription elongation factor, Elongin A (EloA

118 Termination of RNA polymerase II (Pol II) transcription is an important step in the transc

119 mechanistic by-product of RNA polymerase II (Pol II) transcription or biologically meaningful.

120 RNA polymerase II (Pol II) transcription termination by the Nrd1p-Nab3p-Sen

121 m the mammalian genome by RNA polymerase II (Pol II) transcription.

122 ral role in activation of RNA polymerase II (Pol II) transcription.

123 Saccharomyces cerevisiae RNA polymerase II (Pol II) transcripts occurs through two alternative pathw

124 ed levels of transcribing RNA Polymerase II (Pol II) within genes in both species.

125 surrounding transcribing RNA polymerase II (Pol II), and using asymmetric nucleosomes we show that u

126 he genome-wide binding of RNA polymerase II (Pol II), TaDa can also identify transcribed genes in a c

127 ide approach for studying RNA polymerase II (Pol II)-mediated transcription in human cells at single-

128 RNA polymerase II (Pol II)-transcribed genes embedded within the yeast rDNA

129 clusively associated with RNA polymerase II (Pol II)-transcribed genes, but is not an unambiguous mar

130 moter-proximal pausing by RNA polymerase II (Pol II).

131 teraction between p53 and RNA polymerase II (Pol II).

132 iption factors (GTFs) and RNA polymerase II (Pol II).

133 promoter-proximal paused RNA polymerase II (Pol II).

134 at block translocation of RNA polymerase II (Pol II).

135 serum stimulation, a stereotyped increase in Pol II cluster lifetime correlates with a proportionate

136 , however, does not reflect the increases in Pol II density, indicating a global reduction in elongat

137 hown to enter the nucleus and participate in Pol II transcription.

138 s elongation-licensing signals, resulting in Pol II accumulation at the +2 nucleosome and reduced tra

139 raction of p53 and Pol II leads to increased Pol II elongation activity.

140 onal splicing and poly(A) signal-independent Pol II termination of lincRNAs as compared to pre-mRNAs.

141 hat can be effectively rescued by inhibiting Pol II elongation.

142 However, in contrast to Pol IV, Pol II is inefficient at disrupting rolling-circle synth

143 , and found a coactivator role of MTA1/c-Jun/Pol II coactivator complex upon the IGFBP3 transcription

144 n unclear whether over-expression of labeled Pol II under an exogenous promoter may have played a rol

145 Limiting Pol II function with low ATP concentrations shifted the

146 dispensable for establishing or maintaining Pol II pausing but is critical for the release of paused

147 nits and thus probably contribute to a major Pol II binding site.

148 g of Mediator to Pol II to form the Mediator-Pol II holoenzyme.

149 ed on random insertions of exogenous, mutant Pol II coupled with the degradation of endogenous Pol II

150 In contrast to model predictions, mutated Pol II retains normal sensitivity to altered nucleotide

151 uss new roles for ncRNAs, as well as a novel Pol II RNA-dependent RNA polymerase activity that regula

152 Our results indicate that the ability of Pol II to pass the first nucleosome is increased when th

153 te, hydrogen peroxide causes accumulation of Pol II near promoters and enhancers that can best be exp

154 leading to promoter-proximal accumulation of Pol II.

155 We find that alteration of Pol II catalytic rate, either fast or slow, leads to dec

156 ch, which was associated with alterations of Pol II-CTD phosphorylation at the target loci.

157 ermination signals influence the behavior of Pol II at chromatin obstacles, and establish that common

158 subunits, bridging the DNA-binding cleft of Pol II proximal to the upstream DNA entry site.

159 Here we report a stable ternary complex of Pol II, the replicative polymerase Pol III core complex

160 The size and complexity of Pol II, TFIID, and TFIIH have precluded their reconstitu

161 merase, Pol IV, increasing concentrations of Pol II displace the Pol III core during DNA synthesis in

162 riptional and posttranscriptional control of Pol II genes.

163 ila CBP inhibition results in "dribbling" of Pol II from the pause site to positions further downstre

164 little is known about the in vivo effect of Pol II pausing on vertebrate development.

165 disassembly before productive elongation of Pol II is achieved at most genes in the yeast genome.

166 1 and consequently reduces the engagement of Pol II in transcriptional elongation, leading to promote

167 ranscription that enhances the engagement of Pol II into transcriptional elongation) to the coding se

168 nd V clearly evolved as specialized forms of Pol II, but their catalytic properties remain undefined.

169 gress of splicing catalysis as a function of Pol II position.

170 ructurally regulate DNA-binding functions of Pol II via the clamp domain, thereby providing insights

171 experiments reveal that the interactions of Pol II and Pol III with beta allow for rapid exchange du

172 which reveals the exact genomic locations of Pol II.

173 Pase domain promotes the forward movement of Pol II, and elucidate key roles for Rad26 in both TCR an

174 ts (pre-snRNAs), and alters the occupancy of Pol II at snRNA loci.

175 P-seq allowed transcriptional orientation of Pol II to be determined, which may be useful near promot

176 inding, mediate promoter-proximal pausing of Pol II, and/or interact with Pol II to modulate transcri

177 sm for inducing promoter-proximal pausing of Pol II.

178 that P-TEFb-mediated Ser2 phosphorylation of Pol II is dispensable for pause release.

179 point control occurs only in the presence of Pol II-TFIIF.

180 Despite the prevalence of Pol II pausing across the metazoan genomes, little is kn

181 at H3K14R doesn't affect the recruitment of Pol II repressor RENT (regulator of nucleolar silencing

182 mbryos as a model to investigate the role of Pol II pausing in vertebrate organogenesis.

183 To elucidate the role of Pol II poising in B cell activation, we compared Pol II

184 applied to the study of the full spectrum of Pol II transcriptional activities, including the product

185 erminal domain (CTD) of the large subunit of Pol II has been established, but the molecular details o

186 eracts with the phosphorylated C-terminus of Pol II (CTD-interacting domain, CID).

187 eals that Rad26 binds to the DNA upstream of Pol II, where it markedly alters its path.

188 PIP-seq detected divergently oriented Pol II at both coding and noncoding promoters, as well a

189 Therefore, we dissected the human p53/Pol II interaction via single-particle cryo-electron mic

190 Furthermore, the p53/Pol II cocomplex displays a closed conformation as defin

191 anscription factors, PcG proteins and paused Pol II states, these data identify a two-step mechanism

192 ption pausing factor M1BP, containing paused Pol II and enriched with promoter-proximal Polycomb Grou

193 promoter-proximal regions containing paused Pol II.

194 ong support for the residence time of paused Pol II elongation complexes being much shorter than esti

195 ression by controlling the release of paused Pol II in a PAF1-dependent manner.

196 k9 and cyclin T1, promotes release of paused Pol II into elongation, but the precise mechanisms and t

197 tor 1 (PAF1) modulates the release of paused Pol II into productive elongation.

198 ng but is critical for the release of paused Pol II into the gene body at a subset of highly activate

199 d enhancers attenuates the release of paused Pol II on PAF1 target genes without major interference i

200 P and GAGA factor have high levels of paused Pol II, a unique chromatin signature, and are highly exp

201 uction in PcG binding, the release of paused Pol II, increases in promoter H3K4me3 histone marks and

202 of RNA polymerase II at the promoter (paused Pol II) has emerged as a widespread and conserved mechan

203 (CBP) in regulating promoter-proximal paused Pol II.

204 We propose that paused Pol II helps prevent new initiation between transcriptio

205 Here, we show that the release of the paused Pol II is cooperatively regulated by multiple P-TEFbs wh

206 r, it remains largely unclear how the paused Pol II is released in response to stimulation.

207 super elongation complexes (SECs) to paused Pol II to overcome this restriction.

208 ription factors play in transitioning paused Pol II into productive Pol II is, however, little known.

209 e findings reveal a common core to pervasive Pol II initiation throughout the human genome.

210 s through interaction with S2-phosphorylated Pol II and nascent RNA.

211 k H3K9me2 and by reduction in RNA polymerase Pol II occupancy.

212 Of the three, DNA polymerase (Pol) II remains the most enigmatic.

213 ting their capacity to stall RNA polymerase (Pol) II and trigger transcription-coupled nucleotide exc

214 scription through chromatin, RNA polymerase (Pol) II associates with elongation factors (EFs).

215 arboxy-terminal domain (CTD) RNA polymerase (Pol) II formation on the promoters of IRF1, IRF7, and RI

216 Saccharomyces cerevisiae RNA polymerase (Pol) II locates transcription start sites (TSS) at TATA-

217 nucleus and concentrates at RNA polymerase (Pol) II sites, where it acts as a transcriptional cofact

218 promoter-proximal pausing of RNA polymerase (Pol) II, which requires the 4-subunit negative elongatio

219 Pol IIIcore with the translesion polymerases Pol II and Pol IV.

220 transitioning paused Pol II into productive Pol II is, however, little known.

221 he ADP-ribosylation sites on NELF-E promotes Pol II pausing, providing a clear functional link betwee

222 transcription initiation, promoter-proximal Pol II pause release, and transcription termination; how

223 of P-TEFb recruitment and promoter-proximal Pol II pausing.

224 While critical in recruiting Pol II to the promoter, the role transcription factors p

225 s MyoD induces histone acetylation, recruits Pol II, and robustly activates gene transcription.

226 in cofactor mutants was coupled with reduced Pol II occupancies for the Gcn4 transcriptome and the mo

227 hereby providing insights into p53-regulated Pol II transcription.

228 expressed uninduced genes, but the relative Pol II levels at most genes were unaffected or even elev

229 tivation as the result of PAF1 loss releases Pol II from paused promoters of nearby PAF1 target genes

230 promoter may have played a role in reported Pol II dynamics in vivo.

231 RNA Pol II was strongly blocked by a 3d-Napht-A analog but b

232 d for stable CDK9 binding, phospho-Ser 2 RNA Pol II formation, and histone acetyltransferase activity

233 ogs, into DNA oligonucleotides to assess RNA Pol II transcription elongation in vitro.

234 f DNA alkylation impair transcription by RNA Pol II in cells and with the isolated enzyme and unravel

235 Consistent with this conclusion, RNA Pol II phosphorylated at Ser2 of its CTD is detected at

236 ndently regulates CDK9/phospho-Ser 2 CTD RNA Pol II recruitment to the IRF3-dependent IFN-stimulated

237 These results show how RNA Pol II copes with minor-groove DNA alkylation and establ

238 minantly comprised of RNA Polymerase II (RNA Pol II) transcriptional machinery and we demonstrate Psi

239 ing the mechanisms of RNA polymerase II (RNA Pol II)-based transcriptional initiation and discuss the

240 confirmed known protein partners (Ku70, RNA Pol II, p15RS) and discovered several novel associated p

241 is a higher level of CTD Ser2P modified RNA Pol II near CTCF peaks relative to the Ser5P form in the

242 iption by facilitating the elongation of RNA Pol II and preventing silenced chromatin on the viral ge

243 the reduced levels of phosphorylation of RNA Pol II at Ser2 observed at 2- or 4-cell stage of embryos

244 Ankrd26 promoter and loss of binding of RNA Pol II at the Ankrd26 Transcription Start Site (TSS).

245 2P but increased Ser5P modified forms of RNA Pol II on viral genes.

246 he isolated enzyme and unravel a mode of RNA Pol II stalling that is due to alkylation of DNA in the

247 he beta-globin promoter to eliminate the RNA Pol II PIC by deleting the TATA-box resulted in loss of

248 Here we tested the contributions of the RNA Pol II pre-initiation complex (PIC), mediator and cohesi

249 hibitory activity of SBVDeltaNoLS toward RNA Pol II transcription is impaired.

250 roblasts, we observe that short-lived (~8 s) Pol II clusters correlate with basal mRNA output.

251 suggest that Cdk12 acts as a gene-selective Pol II kinase that engages a global shift in gene expres

252 ter gene are increased in both fast and slow Pol II mutant strains and the magnitude of half-life cha

253 ne expression defects for both fast and slow Pol II mutants.

254 ngs suggest that previous exogenously tagged Pol II faithfully recapitulated the endogenous polymeras

255 iption is considerably more error-prone than Pols II or V, which may be tolerable in its synthesis of

256 r establishing memory in this model but that Pol II itself is not retained as part of the memory mech

257 ly developed ChIP-nexus method, we find that Pol II pausing inhibits new initiation.

258 Ultimately we found that Pol II, TATA-binding protein, TFIIB and TFIIF can form a

259 Our results reveal that Pol II backtracking occurs in a stepwise mode where two

260 Our studies show that Pol II pausing is an important contributor to BRCA1-asso

261 bined with prior work, our results show that Pol II transcription plays an important role in TSS sele

262 Previously, we showed that Pol II-associated factor 1 (PAF1) modulates the release

263 sing mNET-seq, we have previously shown that Pol II pauses at both ends of protein-coding genes but w

264 this transcriptional burst, suggesting that Pol II pausing plays a dominant role in gene regulation.

265 nd impair closing of the trigger loop in the Pol II active center and polymerase translocation into t

266 actively threading the downstream DNA in the Pol II PIC.

267 matin association of many EFs, including the Pol II serine 2 kinases Ctk1 and Bur1 and the histone H3

268 nformation as defined by the position of the Pol II clamp domain.

269 y to the serine-5-phosphorylated form of the Pol II CTD, both in the presence and in the absence of v

270 Analysis of the Pol II pre-initiation complex on immobilized chromatin t

271 d to exert complex downstream effects on the Pol II transcriptome, affecting the general regulation o

272 The lack of structures of CSB or the Pol II-CSB complex has hindered our ability to address t

273 Production of snR-DPGs required the Pol II snRNA promoter (PIIsnR), and CPL4RNAi plants show

274 n of the three states in this study with the Pol II system suggests that a ratchet motion of the Core

275 Next, RNA derived from within the Pol II complex is size fractionated and Illumina sequenc

276 Thus Pol II poising does not only mark genes for rapid expres

277 transcription, with M1BP binding leading to Pol II recruitment followed by AbdA targeting, which res

278 n, we show that binding of human Mediator to Pol II depends on the integrity of a conserved "hinge" i

279 step in activation is binding of Mediator to Pol II to form the Mediator-Pol II holoenzyme.

280 est that binding of free viral polymerase to Pol II late in infection may trigger Pol II degradation.

281 o chromatin regions that are in proximity to Pol II and are highly associated with transcripts abunda

282 ith the subgroup of nucleosomes resistant to Pol II inhibition.

283 bits high fidelity transcription, similar to Pol II, suggesting a need for Pol V transcripts to faith

284 al RNA polymerase in the context of vRNPs to Pol II early in infection facilitates cap snatching, whi

285 nslocation of downstream promoter DNA toward Pol II.

286 We tracked Pol II occupancy genome-wide in mammalian cells progress

287 crosslink to RNA emerging from transcribing Pol II in the yeast Saccharomyces cerevisiae.

288 ontributes to EF recruitment to transcribing Pol II.

289 rase to Pol II late in infection may trigger Pol II degradation.

290 ivate gene transcription, themselves undergo Pol II-mediated transcription, but our understanding of

291 Unexpectedly, Pol II transcription of the transgene was required for e

292 We show that splicing is 50% complete when Pol II is only 45 nt downstream of introns, with the fir

293 play Pol II promoter-proximal pausing, while Pol II recruitment and Pol II pausing are not correlated

294 We found that while Pol II poised genes generally overlap functionally among

295 t known to rely on Thr4 for association with Pol II.

296 imal pausing of Pol II, and/or interact with Pol II to modulate transcription.

297 f the PCF11 CID weakens its interaction with Pol II.

298 on, DSP1 binds snRNA loci and interacts with Pol-II in a DNA/RNA-dependent manner.

299 ns: Myf5 induces histone acetylation without Pol II recruitment or robust gene activation, whereas My

300 To investigate a potential role of yeast Pol II transcription in TSS scanning, HIS4 promoter deri