ライフサイエンスコーパス: Pol

1 Pol beta Asn279 and Arg283 are the critical active site

2 Pol delta binds to proliferating cell nuclear antigen (P

3 Pol delta is also crucial for efficient recoupling of le

4 Pol delta is anchored to one of the three PCNA monomers

5 Pol gamma is the only DNA polymerase found in mitochondr

6 Pol I elongation complexes are less stable than Pol II e

7 Pol II also maintains low poising at inactive promoters

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

9 Pol II then initiates relocation to future gene targets

10 Pol III is a determinant of cellular growth and lifespan

11 Pol IV is expressed at increased levels in E. coli cells

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

13 mental defects cluster in hotspots affecting Pol III stability and/or biogenesis, whereas mutations a

14 eldin (SHLD1-3) or CST-DNA polymerase alpha (Pol-alpha) in BRCA1-deficient cells restores HDR and PAR

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

16 loss of p300-dependent H3K27 acetylation and Pol 2-dependent eRNA transcription.

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

18 s PCNA at the DNA nick generated by FEN1 and Pol delta.

19 o N (2)-alkyl-dG lesions was error-free, and Pol nu and Pol theta were dispensable for their replicat

20 st that RNA polymerases I and III (Pol I and Pol III) are the only enzymes that directly mediate the

21 der identical conditions, purified Pol I and Pol III, but not Pol II, could transcribe nucleosomal te

22 somal barrier with those of yeast Pol II and Pol III.

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

24 levels and promoting recruitment of MYB and Pol II.

25 nowledge about the involvement of Pol nu and Pol theta in bypassing alkylated guanine lesions in huma

26 n about the roles of polymerase (Pol) nu and Pol theta in translesion synthesis (TLS) in cells.

27 We found that Pol nu and Pol theta promote TLS across major-groove O (6)-alkyl-dG

28 Simultaneous ablation of Pol nu and Pol theta resulted in diminished mutation frequencies fo

29 yl-dG lesions was error-free, and Pol nu and Pol theta were dispensable for their replicative bypass.

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

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

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

33 DNA polymerases theta (Pol theta) and beta (Pol beta) as mediators of alternative nonhomologous end-

34 Here we describe a novel interaction between Pol delta and LigI that is critical for Okazaki fragment

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

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

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

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

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

40 oligonucleotide (a six-mer in our study) by Pol eta providing a barrier to further elongation of the

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

42 -dependent and -independent transcription by Pol III.

43 the 3.2- angstrom cryo-EM structure of S.c. Pol delta in complex with primed DNA, an incoming ddTTP,

44 cription is observed in cancer and causative Pol III mutations have been described in neurodevelopmen

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

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

47 redominantly to the WH1 domain of the citrus Pol III subunit C34 (CsC34) and that its phosphoregulato

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

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

50 , we show that POLR3G and POLR3GL containing Pol III complexes bind the same target genes and assume

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

52 its of the replicative DNA polymerase delta (Pol delta) as promoters of Alt-NHEJ that results in more

53 In eukaryotes, DNA polymerase delta (Pol delta) bound to the proliferating cell nuclear antig

54 racts with the enzymes DNA polymerase delta (Pol delta), flap endonuclease 1 (FEN1) and DNA ligase I

55 icases in human cells, DNA polymerase delta (Pol delta), with an error-prone variant allows increased

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

57 interaction with the catalytic domain of DNA Pol e.

58 at the Dpb3-Dpb4 subunits bridge the two DNA Pol modules of Pol2, holding them rigid.

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

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

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

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

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

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

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

66 DNA polymerase epsilon (Pol epsilon) is required for genome duplication and tumo

67 Recruitment of DNA polymerase eta (Pol eta) and other Y-family TLS polymerases to damaged D

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

69 Pol2 is a fusion of two B-family Pols; the N-terminal Pol module is catalytic and the C-t

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

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

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

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

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

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

76 plication, serving as a template for Gag/Gag-Pol translation and as a genome for the progeny virion.

77 ted 30 rhesus macaques with Ad26-SIV Env/Gag/Pol and SIV Env gp140 protein vaccines and assessed the

78 omosome 15, encodes the DNA polymerase gamma(Pol gamma).

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

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

81 In the pollen grain, Pol IV is also required for the accumulation of 21/22-nu

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

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

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

85 the DNA substrate is handed back to the HiFi Pol after bypass of 8-oxoG.

86 position where the TLS Pol ends and the HiFi Pol resumes (i.e. the length of the TLS patch) has not b

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

88 quantification of fingers movement in human Pol beta reported here provide new insights into the del

89 g and prechemistry fingers movement of human Pol beta.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 veals its unexpected effect on incorporating Pol epsilon into the four-member pre-loading complex dur

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

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

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

124 ay lead to cancer and genetic instabilities, Pol beta has been extensively studied, especially its me

125 thaliana), DNA-dependent RNA polymerase IV (Pol IV) is required for the formation of transposable el

126 subunit of plant-specific RNA polymerase IV (Pol IV), which is required for RNA-directed DNA methylat

127 Second, using acceptor-labeled Pol beta and donor-labeled DNA, we visualized dynamic fi

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

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

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

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

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

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

134 Simultaneous ablation of Pol nu and Pol theta resulted in diminished mutation fre

135 er escape and early elongation activities of Pol II.

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

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

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

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

140 main of Pol3, suggesting that all aspects of Pol delta replication are important to human health and

141 work sheds light on the structural basis of Pol delta's activity in replicating the human genome.

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

143 ssembly of defective initiation complexes of Pol III.

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

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

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

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

148 Depletion of Pol nu alone reduced mutations only for O (6)-nBu-dG, an

149 or PIAS1- and STUbL-mediated displacement of Pol eta from DNA damage sites.

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

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

152 binding regions, suggesting an impairment of Pol III cytosolic viral DNA-sensing.

153 critical knowledge about the involvement of Pol nu and Pol theta in bypassing alkylated guanine lesi

154 However, the genetic and functional links of Pol III to innate immunity in humans remain largely unkn

155 ions only for O (6)-nBu-dG, and sole loss of Pol theta attenuated the mutation rates for O (6)-nBu-dG

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

157 tions, we studied the effect of oxidation of Pol gamma on replication errors.

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

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

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

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

162 The reciprocation of Pol activities at this intermediate indicates a defined

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

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

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

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

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

168 is, perhaps explaining the essential role of Pol IV in pollen development in Capsella.

169 Despite this proposed role of Pol IV, its loss of function in Arabidopsis does not cau

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

171 The stalling of Pol eta directly past the ICL is attributed to its autoi

172 POLR3E gene, coding for a protein subunit of Pol III, in a child with recurrent and systemic viral in

173 ut of NRPD1, encoding the largest subunit of Pol IV, in the Brassicaceae species Capsella (Capsella r

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

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

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

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

178 Upregulation of Pol III transcription is observed in cancer and causativ

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

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

181 ain the regulation of the oxidation state on Pol delta activity, possibly useful during cellular oxid

182 , by 2-3 fold, compared to Pol zeta alone or Pol eta.

183 reviously shown following targeting of other Pol zeta-proteins, suggesting that Pol zeta-dependent an

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

185 ard, DNA polymerase theta differs from other Pols in that whereas purified Poltheta misincorporates a

186 ination positively regulates TLS to overcome Pol delta inhibition.

187 The oxidized Pol gamma becomes editing-deficient, displaying a 20-fol

188 Rev1-Pol zeta, and particularly Pol zeta alone showed a tendency to stall before the ICL

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

190 The DNA polymerase (Pol) delta of Saccharomyces cerevisiae (S.c.) is compose

191 he eukaryotic leading strand DNA polymerase (Pol) epsilon contains 4 subunits, Pol2, Dpb2, Dpb3 and D

192 use the high-fidelity (HiFi) DNA polymerase (Pol) to stall.

193 much is known about the roles of polymerase (Pol) nu and Pol theta in translesion synthesis (TLS) in

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

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

196 as the central regulator of RNA polymerase (Pol) III activity.

197 RNA polymerase (Pol) III has a noncanonical role of viral DNA sensing in

198 In eukaryotes, RNA Polymerase (Pol) III is specialized for the transcription of tRNAs a

199 vation of the leading strand DNA polymerase, Pol epsilon, dNTP depletion, and chemical inhibition of

200 isingly, the main lagging-strand polymerase, Pol delta, binds the leading strand upon uncoupling and

201 e monophosphates (rNMPs) by DNA polymerases (Pol) into DNA.

202 translesion synthesis (TLS) DNA polymerases (Pols) are retained in their cellular roles.

203 DNA polymerases (Pols) provide roles in both replication of the genome an

204 three nuclear DNA-dependent RNA polymerases (Pols) responsible for synthesizing all RNA required by t

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

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

207 r extension utilised by closely related Prim-Pols.

208 on cryo-EM structure of the human processive Pol delta-DNA-PCNA complex in the absence and presence o

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

210 Nuclear GAPDH promotes Pol beta polymerase activity and increases base excision

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

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

213 ferently in human cells than in the purified Pol establishes a new paradigm for DNA polymerase functi

214 The active site in the quaternary Pol mu complex is poised for catalysis and nucleotide in

215 9 activity and viral DNA replication reduced Pol II on the viral genome and restricted much of the re

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

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

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

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

220 To understand how the mtDNA replicase, Pol gamma, can give rise to elevated mutations, we studi

221 dNTP pools slow DNA synthesis by replicative Pols and provoke the incorporation of high levels of rNM

222 propose a mechanism for how CsMAF1 represses Pol III transcription and how phosphorylation controls t

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

224 Rev1-Pol zeta, and particularly Pol zeta alone showed a tende

225 The Rev1-Pol zeta complex was most efficient in complete bypass s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

241 o Pol III, establishing that Maf1 sequesters Pol III elements involved in transcription initiation an

242 visualized dynamic fingers closing in single Pol beta-DNA complexes upon addition of complementary nu

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

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

245 hat Pol alpha-primase and the lagging-strand Pol delta can be re-used within the replisome to support

246 ta suggest that the examined domain supports Pol epsilon catalytic activity and symmetric movement of

247 l Pol module is catalytic and the C-terminal Pol module is non-catalytic.

248 fusion of two B-family Pols; the N-terminal Pol module is catalytic and the C-terminal Pol module is

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

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

251 ing proteomic profiling, we demonstrate that Pol eta is targeted for multisite SUMOylation, and that

252 (2020) also demonstrate that Pol II termination is not observed with gapmers targetin

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

254 We found that Pol eta undergoes DNA damage- and protein inhibitor of a

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

256 We found that Pol nu and Pol theta promote TLS across major-groove O (

257 and LigI remain on the DNA, indicating that Pol delta and FEN1 dissociate during 5' end processing a

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

259 merase activity in replication and show that Pol alpha-primase and the lagging-strand Pol delta can b

260 a doubly labeled DNA construct, we show that Pol beta bends the gapped DNA substrate less than indica

261 We show that Pol gamma exo domain is far more sensitive to oxidation

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

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

264 the polymerase-DNA complex, suggesting that Pol beta, when bound to a lesion, has a strong commitmen

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

266 of other Pol zeta-proteins, suggesting that Pol zeta-dependent and -independent roles of Rev7 are re

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

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

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

270 rticularly, we demonstrate redundancy of the Pol alpha-primase DNA polymerase activity in replication

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

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

273 n Dbp2 directs leading ssDNA from CMG to the Pol epsilon active site.

274 udies have implicated DNA polymerases theta (Pol theta) and beta (Pol beta) as mediators of alternati

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

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

277 The exact position where the TLS Pol ends and the HiFi Pol resumes (i.e. the length of th

278 diate indicates a defined position where TLS Pol extension is limited and where the DNA substrate is

279 ion cryo-EM structure of yeast Maf1 bound to Pol III, establishing that Maf1 sequesters Pol III eleme

280 e bypass synthesis, by 2-3 fold, compared to Pol zeta alone or Pol eta.

281 creases CsMAF1 affinity to CsC34, leading to Pol III derepression, and that Ser 45, found only in pla

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

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

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

285 All cells express a range of translesion Pols, but little work has examined their function in par

286 Unexpectedly, Pol delta binds only one subunit of the PCNA trimer.

287 a tendency to stall before the ICL, whereas Pol eta stalled just after insertion across the ICL.

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

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

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

291 ogether, these data support a model in which Pol delta promotes Alt-NHEJ in human cells at DSBs, incl

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

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

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

295 ol II transcription robustly interferes with Pol III function at specific tRNA genes.

296 e a 3.5- angstrom cryo-EM structure of yeast Pol epsilon revealing that the Dpb3-Dpb4 subunits bridge

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

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

299 DNA polymerase zeta (Pol zeta) and Rev1 are essential for the repair of DNA i

300 nscriptase, translesion DNA polymerase zeta (Pol zeta) plays a major role in R-TDR, and it is essenti