ライフサイエンスコーパス: Pol II

1 Pol II also maintains low poising at inactive promoters

2 Pol II crossing dynamics are complex, displaying pauses

3 Pol II pausing is observed in most expressed genes acros

4 Pol II processivity is impaired in diauxic cells, but st

5 Pol II then initiates relocation to future gene targets

6 Pol II, assisted by the neurodegeneration-associated enz

7 s lack the A49-A34.5 heterodimer and adopt a Pol II-like conformation, in which the A12.2 C-terminal

8 Our results identified SIRT6 as a Pol II promoter-proximal pausing-dedicated histone deace

9 sh an important physiological function for a Pol II regulatory factor (Gdown1) in the maintenance of

10 highly specific guide RNA production from a Pol-II promoter.

11 ide, with nascent RNAs at most of the active Pol II transcription sites and at some Pol III-transcrib

12 ously reported dual RNA polymerase activity (Pol II/III) for the human H1 promoter and demonstrated t

13 AID-Pol II mutations are strongly favored in WRC and WGCW ov

14 h PBAP (SWI/SNF) to open chromatin and allow Pol II to be recruited.

15 he extent of promoter sensitivity to altered Pol II activity in ways that are predicted by a scanning

16 Although Pol II is a complex, 12-subunit enzyme, it lacks the abi

17 Loss of ETO2 elevates LDB1, MED1 and Pol II in the locus and facilitates fetal gamma-globin/L

18 ontrary to current models, however, mMED and Pol II are dispensable to physically tether regulatory D

19 levels and promoting recruitment of MYB and Pol II.

20 ompanied by changes at genic nucleosomes and Pol II redistribution.

21 s to decreased PRC1 and PRC2 recruitment and Pol II activation into a productive elongation state, ac

22 etermined genome-wide SOX2-bound regions and Pol II-mediated long-range chromatin interactions in bra

23 on resulted in the binding of TBP, TAF1, and Pol II to previously silent late promoters.

24 resulted in reduced binding of Sp1, TBP, and Pol II to early promoters.

25 rgo dynamic rearrangement and disassembly as Pol II moves away from the start site of transcription a

26 sed, a characteristic feature of backtracked Pol II.

27 Because Pol II transcribes multiple gene types, its termination

28 criptional start site, while beta genes bore Pol II more evenly across gene bodies.

29 indicating that repression of tRNA genes by Pol II is dynamically regulated.

30 ulatory event in transcription initiation by Pol II, and it phosphorylates the regulatory T-loop of C

31 viral transcription is regulated not only by Pol II recruitment to viral genes but also by control of

32 motes efficient transcription termination by Pol II through interaction with CBC-ARS2 and NELF/DSIF,

33 hese disruptive sincRNAs can be unleashed by Pol II inhibition, senataxin loss, Ewing sarcoma or locu

34 ply that transcriptional regulation of wg by Pol II pausing factor M1BP may be one of the important r

35 Although numerous different obstacles cause Pol II stalling or arrest, the cell somehow distinguishe

36 Removal of cohesin/Pol II from chromosome arms in prophase is important for

37 We combined Pol II chromatin immunoprecipitation sequencing (ChIP-se

38 the pre-initiation complex (PIC), comprising Pol II and the general transcription factors.

39 der-wound DNA from Top2, while Top2 confines Pol II and Top1 at coding units, counteracting transcrip

40 similar to that observed in cells containing Pol II derivatives with slow elongation rates.

41 Here we quantified Mediator-controlled Pol II kinetics by coupling rapid subunit degradation wi

42 pt5 dephosphorylation is required to convert Pol II into a viable target for the Xrn2 terminator exon

43 hich correlates with Spt5 dephosphorylation. Pol II deceleration and Spt5 dephosphorylation require p

44 the current knowledge of how these different Pol II stalling contexts are distinguished by the cell,

45 Furthermore, PTEN re-distributes Pol II occupancy across the genome and possibly impacts

46 applying our approach to analyze Drosophila Pol II transcriptional components.

47 econstitute AID-catalyzed deamination during Pol II transcription elongation in conjunction with DSIF

48 n the addition site and is not stable during Pol II translocation after the chemistry step.

49 stream from this process to ensure efficient Pol II pause release and transition to productive elonga

50 ent compensatory feedback loop that elevated Pol II pause release rates across the genome.

51 C-terminal domain and dismantles elongating Pol II from DNA in vitro.

52 leted cells exhibit low levels of elongating Pol II and high levels of terminating Pol II, consistent

53 d RNA by XRN2 and dissociation of elongating Pol II.

54 nd cohesin is necessary to retain elongating Pol II at centromeres.

55 ically, Gdown1 is associated with elongating Pol II on the highly expressed genes and its ablation le

56 In Drosophila embryo, Pol II pausing is known to regulate the developmental co

57 wing that ChIP-nexus captures the endogenous Pol II pausing on transfected plasmids.

58 scription elongation factors that facilitate Pol II nucleosome bypass without hydrolyzing ATP.

59 After fertilization, Pol II is preferentially loaded to CG-rich promoters and

60 c assessment and factor-binding analysis for Pol II, TBP, TAF1, and Sp1 to assess the effect genome r

61 The structural basis for Pol II transcription regulation has advanced rapidly in

62 h replication proteins but are defective for Pol II recruitment.

63 he model that TFIIB release is important for Pol II to successfully escape the promoter as initiating

64 te key predictions of the scanning model for Pol II initiation in yeast, which we term the shooting g

65 ed a core of essential subunits required for Pol II recruitment genome-wide.

66 DNA replication is required to maintain full Pol II occupancy on viral DNA and to promote elongation

67 Furthermore, Pol II occupancy markedly increased near cleavage and po

68 r variants and explored their use as general Pol II promoters for protein expression.

69 At many genes, Pol II pauses stably in early elongation, remaining enga

70 echanism of over a dozen factors that govern Pol II initiation (e.g., TFIID, TFIIH, and Mediator), pa

71 e CSB facilitates gene expression by helping Pol II bypass chromatin obstacles while maintaining thei

72 ATP-dependent processivity factor that helps Pol II across a nucleosome barrier.

73 Hence, Pol II plays a direct and central role in the gene-speci

74 n compartments (RCs) efficiently enrich host Pol II into membraneless domains, reminiscent of liquid-

75 At 6 hpi, Pol II increased on gamma(1) and gamma(2) genes while Po

76 Human Pol II promoters with slow TBP dissociation preferential

77 Here we analyse the human Pol II core promoter and use machine learning to generat

78 Our data more clearly define the human Pol II promoter: a TFIID binding site with built-in down

79 iation, large clusters of hypophosphorylated Pol II rapidly disassembled upon Mediator degradation.

80 f RNA Pol II) in living cells, we identified Pol II as a direct gene-specific regulator of tRNA trans

81 downregulation results in RNA polymerase II (Pol II) accumulation at the 3' end of genes, correlating

82 ler binding and increased RNA polymerase II (Pol II) activity.

83 RNA polymerase II (Pol II) and its general transcription factors assemble o

84 use sperm are occupied by RNA polymerase II (Pol II) and Mediator.

85 cription system with purified polymerase II (Pol II) and Rad26, a yeast ortholog of CSB, to study the

86 eviction is dependent on RNA Polymerase II (Pol II) and the Kin28/Cdk7 kinase, which phosphorylates

87 RNA Polymerase II (Pol II) and transcription factors form concentrated hubs

88 The journey of RNA polymerase II (Pol II) as it transcribes a gene is anything but a smoot

89 transcription factor and RNA polymerase II (Pol II) association with viral DNA prior to the onset of

90 ic mRNA-encoding genes by RNA polymerase II (Pol II) begins with assembly of the pre-initiation compl

91 tigated the landscapes of RNA polymerase II (Pol II) binding in mouse embryos.

92 The RNA polymerase II (Pol II) core promoter is the strategic site of convergen

93 n correlates with altered RNA polymerase II (Pol II) distribution.

94 Pausing of RNA polymerase II (Pol II) during early transcription, mediated by the nega

95 covers a rapid release of RNA polymerase II (Pol II) from a group of promoters.

96 The transition of RNA polymerase II (Pol II) from initiation to productive elongation is a ce

97 f the RPB1 subunit of the RNA polymerase II (Pol II) has been revived in recent years, owing to its n

98 on involve the pausing of RNA polymerase II (Pol II) in early elongation, and the controlled release

99 transcriptionally active RNA polymerase II (Pol II) in mitosis.

100 re we show, however, that RNA polymerase II (Pol II) inside human nucleoli operates near genes encodi

101 moter-proximal pausing of RNA polymerase II (Pol II) is a critical step in transcriptional regulation

102 Transcription by RNA polymerase II (Pol II) is carried out by an elongation complex.

103 -terminal domain (CTD) of RNA polymerase II (Pol II) is composed of repeats of the consensus YSPTSPS

104 dies provide snapshots of how polymerase II (Pol II) is stalled by a nonbulky Gh lesion in a stepwise

105 cleus coopting the host's RNA Polymerase II (Pol II) machinery for production of viral mRNAs culminat

106 Condensates containing RNA polymerase II (Pol II) materialize at sites of active transcription.

107 nifests as a reduction of RNA polymerase II (Pol II) occupancy downstream of transcription start site

108 nation (H2Bub) facilitate RNA polymerase II (Pol II) passage through chromatin, yet it is not clear h

109 The phenomenon of RNA polymerase II (Pol II) pausing at transcription start site (TSS) is one

110 RNA polymerase II (Pol II) pausing is a general regulatory step in transcri

111 RNA polymerase II (Pol II) pausing is a key regulatory step in transcriptio

112 o better understand human RNA polymerase II (Pol II) promoters in the context of promoter-proximal pa

113 tide repeat domain of the RNA polymerase II (Pol II) subunit RPB1, which is an important regulatory e

114 s decrease recruitment of RNA polymerase II (Pol II) to an intron-containing gene, which is rescued b

115 RNA polymerase II (Pol II) transcribes all protein-coding genes and many no

116 RNA polymerase II (Pol II) transcribes hundreds of thousands of transcripti

117 otein 7 (RBM7) stimulates RNA polymerase II (Pol II) transcription and promotes cell viability by act

118 at stimulates the rate of RNA polymerase II (Pol II) transcription elongation in vitro.

119 RNA polymerase II (Pol II) transcription is tightly regulated at promoter-p

120 exon-targeted ASOs cause RNA polymerase II (Pol II) transcription termination in cultured cells and

121 -terminal domain (CTD) of RNA-polymerase II (Pol II), and reduces the expression of key DNA damage re

122 discrete genomic loci by RNA polymerase II (Pol II), resulting in 28 nt short-capped piRNA precursor

123 fluenza RdRP and cellular RNA polymerase II (Pol II), which is the source of nascent capped host RNAs

124 cyte-specific ablation of RNA polymerase II (Pol II)-associated Gdown1 leads to down-regulation of hi

125 gradation of the residual RNA polymerase II (Pol II)-associated RNA by XRN2 and dissociation of elong

126 tment of coactivators and RNA polymerase II (Pol II).

127 e transcribed by cellular RNA polymerase II (Pol II).

128 transcription factors to RNA polymerase II (Pol II).

129 pancy across the genome and possibly impacts Pol II pause duration, release and elongation rate in or

130 shift in a polar fashion upon alteration in Pol II catalytic activity or GTF function.

131 ay is available for measuring the changes in Pol II pausing as a result of altered promoter sequences

132 model in which topoisomerases participate in Pol II promoter-proximal pausing and indicated that DSBs

133 antly, we found that loss of Paf1 results in Pol II elongation rate defects with significant rate com

134 ons by intricate dynamic processes including Pol II pausing, release into elongation and premature te

135 Using an inducible Pol II-degradation system that we previously established

136 transcription allosterically by influencing Pol II translocation.

137 Biochemically, R-loops act as intrinsic Pol II promoters to induce de novo RNA synthesis.

138 n the carboxy-terminal domain of the largest Pol II subunit Rpb1.

139 it, and both modifications greatly lengthen Pol II crossing time.

140 decreasing binding of the GATA2/AR/Mediator/Pol II transcriptional complex, contributing to sensitiz

141 iniature H1/7SK hybrid promoter with minimal Pol II activity, thereby boosting Pol III activity to a

142 In this model, Pol II catalytic activity and the rate and processivity

143 strains with reduced processivity and normal Pol II elongation rates have normal polyadenylation prof

144 ditions, purified Pol I and Pol III, but not Pol II, could transcribe nucleosomal templates.

145 ajor RNA polymerases, and identify nucleolar Pol II as a major factor in protein synthesis and nuclea

146 We reveal a nucleolar Pol-II-dependent mechanism that drives ribosome biogenes

147 er escape and early elongation activities of Pol II.

148 fications is associated with the activity of Pol II during the transcription cycle.

149 ptional repression through the alteration of Pol II phosphorylation states, thereby contributing to o

150 t during the first 3 h reduced the amount of Pol II associated with the viral genome and confined mos

151 More substantial blocking of Pol II translocation can be caused by other physiologica

152 Ddi1 targets, we found the core component of Pol II and show that its genotoxin-induced degradation i

153 a pre-initiation complex (PIC) comprised of Pol II and conserved general transcription factors (GTFs

154 quirement of the full CTD for the control of Pol II activity at endogenous mammalian genes has never

155 of the CTD in the post-initiation control of Pol II.

156 hosphorylates the C-terminal domain (CTD) of Pol II and negative elongation factors to release Pol II

157 prophase is required for the dissociation of Pol II and nascent transcripts, and failure of this proc

158 the hypophosphorylated C-terminal domain of Pol II is incorporated into mediator condensates and tha

159 tes NELF and the carboxyl terminal domain of Pol II-and enrichment of the positive transcription elon

160 ptome, including the first identification of Pol II PPP sites.

161 sion, however, the functional implication of Pol II pausing during later developmental time windows r

162 rminal domain regulates the incorporation of Pol II into phase-separated condensates that are associa

163 osphorylation, thereby causing inhibition of Pol II release from the transcriptional start site.

164 We provide a detailed map of Pol II occupancy on the HSV-1 genome that clarifies feat

165 omponent molecules: hundreds of molecules of Pol II and mediator are concentrated in condensates at s

166 III, whereas the remaining ones are part of Pol II transcripts.

167 Because passage of Pol II through +1 nucleosomes genome-wide would obligate

168 Reversible phosphorylation of Pol II and accessory factors helps order the transcripti

169 ic activity and the rate and processivity of Pol II scanning together with promoter sequence determin

170 substantially enhance the elongation rate of Pol II in vivo.

171 t genes featured exceptionally high rates of Pol II turnover.

172 chromatin remodelers to allow recruitment of Pol II and entry to a promoter-proximal paused state, an

173 egulatory regions, where tight regulation of Pol II activity is necessary for proper ESC differentiat

174 K9 activity nor essential for the release of Pol II into productive elongation.

175 se I (Pol I) transcription and repression of Pol II.

176 Resolution of Pol II blocking can be as straightforward as temporary b

177 opment, accompanied by aberrant retention of Pol II and ectopic expression of one-cell targets upon m

178 mportance of stress-dependent stimulation of Pol II pause release, which enables a pro-survival trans

179 The large subunit of Pol II contains an intrinsically disordered C-terminal d

180 tion rate constants are faster than those of Pol II.

181 m cells, EloA localizes to both thousands of Pol II transcribed genes with preference for transcripti

182 tory complex that regulates transcription of Pol II-dependent genes.

183 Hence, stepwise transition of Pol II occurs when mammalian life begins, and minor ZGA

184 that have enabled a deeper understanding of Pol II transcription mechanisms; we also highlight mecha

185 This arrangement does not depend on Pol II or S phase.

186 igenetic modifications, and their effects on Pol II nucleosome crossing dynamics, is still missing.

187 ther ChIP-seq reveals that global effects on Pol II-binding are mutually rescued by prp5-GAR and spt8

188 Although paused Pol II stability correlates with core promoter elements,

189 rturbed growth conditions, release of paused Pol II at specific loci and chromatin territories favors

190 n transcription, yet the stability of paused Pol II varies widely between genes.

191 the field concerning the stability of paused Pol II, nucleosomes as obstacles to elongation, and pote

192 1 nucleosome is present downstream of paused Pol II.

193 nascent RNA and drive termination of paused Pol II.

194 redistribution of promoter-proximally paused Pol II into gene bodies.

195 Here, we report that paused Pol II can be actively destabilized by the Integrator co

196 Damaged introns with paused Pol II-pS5, TOP2B and XRCC4 are enriched in translocatio

197 romoter classes in S. cerevisiae, we perturb Pol II catalytic activity and GTF function and analyze t

198 -DCAF7 can co-migrate with and phosphorylate Pol II along the myogenic gene loci.

199 of unphosphorylated and Ser5 phosphorylated Pol II around promoter-proximal regions and within the f

200 ranscriptional elongation by RNA polymerase (Pol) II and regulates cell growth and differentiation.

201 and phosphorylated forms of RNA polymerase (Pol) II at the promoter and gene body.

202 -TEFb, a master regulator of RNA polymerase (Pol) II elongation, phosphorylates the C-terminal domain

203 f nuclear damage at sites of RNA polymerase (Pol) II transcription initiation, revealing a novel and

204 y displays rapid turnover at RNA polymerase (Pol) II-transcribed promoters, slow turnover at Pol III

205 mination or degradation of polyubiquitylated Pol II and its associated nascent RNA.

206 We previously reported an activated porcine Pol II elongation complex, EC*, encompassing the human e

207 allows transcript knockdown while preserving Pol II association with the gene body.

208 r-proximal paused state, and also to promote Pol II's transition to productive elongation.

209 precursors associated with promoter-proximal Pol II, resulting in termination of transcription.

210 We image, track, and quantify Pol II with single-molecule resolution, unveiling its dy

211 with deep sequencing to map and to quantify Pol II on the HSV-1(F) genome with single-nucleotide res

212 9 activity and viral DNA replication reduced Pol II on the viral genome and restricted much of the re

213 ssed genes and its ablation leads to reduced Pol II recruitment to these genes, suggesting that Pol I

214 C-terminal domain phosphorylation regulates Pol II partitioning into distinct condensates connected

215 I and negative elongation factors to release Pol II from promoter-proximal pausing.

216 al genome and confined most of the remaining Pol II to alpha gene PPP sites.

217 genome and restricted much of the remaining Pol II to PPP sites.IMPORTANCE These data suggest that v

218 the kinase refractory to MFH290 and restored Pol II CTD phosphorylation and DNA damage repair gene ex

219 leading to H4K16ac loss causes aberrant RNA Pol II recruitment, compromises the 3D organization of t

220 me inhibition on the chromatin state and RNA Pol II transcription.

221 enrichment of anti-WW/SS nucleosomes and RNA Pol II transcriptional levels in mammals (mouse and huma

222 ulatory genetic elements, and eliminates RNA Pol II but not BRD4 phase condensates.

223 imited overall changes in RNA levels for RNA Pol II genes after TbRH2A loss, but increased perturbati

224 s of the anti-WW/SS sequence pattern for RNA Pol II transcription are discussed.

225 early elongation complexes distinct from RNA Pol II pause-release.

226 RNA polymerase II (RNA Pol II) contains a disordered C-terminal domain (CTD) wh

227 recise control of the RNA polymerase II (RNA Pol II) cycle, including pausing and pause release, main

228 eracetylation removes RNA polymerase II (RNA Pol II) from core regulatory genetic elements, and elimi

229 RNA polymerase II (RNA Pol II) is generally paused at promoter-proximal regions

230 driven recruitment of RNA polymerase II (RNA Pol II) to promoters and enhancers.

231 s, we reveal a mechanism that integrates RNA Pol II cycle transitions.

232 show that upon rapid depletion of NELF, RNA Pol II fails to be released into gene bodies, stopping i

233 , guaranteeing continuous progression of RNA Pol II entry to and exit from the pause state.

234 Here, we mapped the locations of RNA Pol II in normal human cells and found that RNA Pol II p

235 dly deplete RPB1 (the largest subunit of RNA Pol II) in living cells, we identified Pol II as a direc

236 stinct chromatin states and key steps of RNA Pol II-mediated transcription in cancer cells.

237 t the Integrator complex can bind paused RNA Pol II and drive premature transcription termination, po

238 nt release of promoter-proximally paused RNA Pol II into productive elongation is essential for gene

239 tment of Ser-5- and Ser-2-phosphorylated RNA Pol II.

240 vels in the gene body reflect productive RNA Pol II elongation of transcripts of genes that are induc

241 Significantly, a loss of proper RNA Pol II targeting to distinct transcription-splicing terr

242 During the heat shock response, RNA Pol II is rapidly released from pausing at heat shock-in

243 aracterization of these sites shows that RNA Pol II pauses at GC-rich regions that are marked by a se

244 II in normal human cells and found that RNA Pol II pauses in a consistent manner across individuals

245 tegrator-bound PP2A dephosphorylates the RNA Pol II C-terminal domain and Spt5, preventing the transi

246 ), interacts with UBR5 and represses the RNA Pol II elongation and RNA synthesis.

247 ound transcription factors (TFs) and the RNA Pol II machinery.

248 sociates with transcribed regions, tunes RNA Pol II transcription levels via impacts on enhancer RNA

249 atin docking, KAP1 first associates with RNA Pol II and then recruits a pathway-specific transcriptio

250 taining protein 4 (BRD4), thus enhancing RNA-Pol II-dependent transcription and inducing metastasis.

251 horylation requires both DNA binding and RNA-Pol-II elongation, we propose that this event acts to cl

252 Immediately downstream of poly(A) sites, Pol II decelerates from >2 kb/min to <1 kb/min, which co

253 In parallel, we also engineered small Pol II-specific H1 promoter variants and explored their

254 odule associates with CPL2, a plant-specific Pol II carboxyl terminal domain (CTD) phosphatase, to fo

255 e elongation factor (NELF), thus stabilizing Pol II promoter-proximal pausing.

256 RTF1 strongly stimulates Pol II elongation, and this requires the latch, possibly

257 gating Pol II and high levels of terminating Pol II, consistent with defects in both termination and

258 omplexes, and Pol I is more error prone than Pol II.

259 I elongation complexes are less stable than Pol II elongation complexes, and Pol I is more error pro

260 highly transcribed and paused genes and that Pol II promoter-proximal pausing sites are enriched in D

261 (2020) also demonstrate that Pol II termination is not observed with gapmers targetin

262 We found that Pol II undergoes 'loading', 'pre-configuration', and 'pr

263 The data indicate that Pol II is recruited to late genes early in infection.

264 ic and causal-association models showed that Pol II pausing at long genes is the main predictor and d

265 Our data suggest that Pol II transcription robustly interferes with Pol III fu

266 among different cell types, suggesting that Pol II promoter-proximal pausing is a common regulatory

267 recruitment to these genes, suggesting that Pol II redistribution may facilitate hepatocyte re-entry

268 y at PPP sites and gene bodies suggests that Pol II is released more efficiently into the bodies of b

269 that extend from the Plus3 domain along the Pol II protrusion and RPB10 to the polymerase funnel.

270 (UIM) abrogates the FACT association and the Pol II arrest, providing a possible link between the tra

271 interactions are necessary for arresting the Pol II elongation at lesions.

272 romatin context progressively changes as the Pol II moves along the guide DNA.

273 Notably, inhibition of minor ZGA impairs the Pol II pre-configuration and embryonic development, acco

274 the bridge helix, a flexible element of the Pol II active site.

275 vestigate whether the phosphorylation of the Pol II C-terminal domain regulates the incorporation of

276 , that the vRNAP subunit Rpo30 resembles the Pol II elongation factor TFIIS, and that NPH-I resembles

277 ures show that Rap94 partially resembles the Pol II initiation factor TFIIB, that the vRNAP subunit R

278 A) factor PCF11, which directly binds to the Pol II C-terminal domain and dismantles elongating Pol I

279 A, creating negative supercoiling within the Pol II cleft to facilitate promoter opening.

280 Thus, Pol II elongation speed is important for poly(A) site se

281 At that time, Pol II on alpha genes accumulated most heavily at promot

282 We find that alterations to Pol II, TFIIB, or TFIIF function widely alter the initia

283 which could impose a considerable barrier to Pol II elongation past TSS-proximal regions.

284 es have revealed how influenza RdRP binds to Pol II and how this binding promotes the initiation of v

285 that the histone deacetylase SIRT6 binds to Pol II and prevents the release of the negative elongati

286 DCAF7 that stabilizes and tethers DYRK1A to Pol II, so that DYRK1A-DCAF7 can co-migrate with and pho

287 the physical proximity of the spliceosome to Pol II, we surveyed the effect of epigenetic context on

288 Approximately 30% of total Pol II relocated to viral genomes within 3 h postinfecti

289 relationship to the activity of transcribing Pol II is not understood.

290 t enable pausing and the events that trigger Pol II release into the gene.

291 iently, but shows increased association when Pol II promoter escape is inhibited.

292 oth enhancer and promoter sequences, whereas Pol II loading rate is primarily modulated by the enhanc

293 ion, but instead represses the rate at which Pol II initiates transcription of highly methylated long

294 creased on gamma(1) and gamma(2) genes while Pol II pausing remained prominent on alpha genes.

295 and its restoration establishes genome-wide Pol II promoter-proximal pausing in PTEN null cells.

296 position and clearance at the subset of wide Pol II promoter NDRs.

297 The RTF1 Plus3 domain associates with Pol II subunit RPB12 and the phosphorylated C-terminal r

298 We show that CSB forms a stable complex with Pol II and acts as an ATP-dependent processivity factor

299 proteins and protein complexes interact with Pol II to regulate its activity.

300 ss a nucleosomal barrier with those of yeast Pol II and Pol III.

301 Such usage of yeast Pol II suggests a general mechanism coupling eukaryotic