ライフサイエンスコーパス: translesion synthesis

1 eloping novel cancer therapeutics to inhibit translesion synthesis.

2 Rev1 is an essential scaffolding protein in translesion synthesis.

3 al repair enzyme recognition, processing and translesion synthesis.

4 tandard DNA structures in a process known as translesion synthesis.

5 cation of the DNA surrounding the lesion and translesion synthesis.

6 s that both prevent and facilitate mutagenic translesion synthesis.

7 lesion and the incoming nucleotide to assist translesion synthesis.

8 roperties of DNA Pol II that facilitate this translesion synthesis.

9 d thus generate active mutasomal complex for translesion synthesis.

10 PCNA plays an essential role in facilitating translesion synthesis.

11 slipped mutagenic intermediate (SMI) during translesion synthesis.

12 A polymerases that can bypass the lesion via translesion synthesis.

13 Rad6-Rad18 complex as the initiating step of translesion synthesis.

14 Y family of DNA polymerases that function in translesion synthesis.

15 kappa functions during the extension step of translesion synthesis.

16 recombination, nonhomologous endjoining and translesion synthesis.

17 ll-characterized Y-family DNA polymerase for translesion synthesis.

18 would encounter during the extension step of translesion synthesis.

19 through an as yet poorly understood role in translesion synthesis.

20 dependent roles in the control of vertebrate translesion synthesis.

21 pa, catalyze the bypass of DNA damage during translesion synthesis.

22 important non-catalytic role in coordinating translesion synthesis.

23 aintaining the DNA-polymerase complex during translesion synthesis.

24 ne pyrimidine dimers during a process termed translesion synthesis.

25 iscrimination without affecting m6G template translesion synthesis.

26 site-induced mutagenesis largely depends on translesion synthesis.

27 tes DNA orientation and translocation during translesion synthesis.

28 about the non-catalytic function of Rev1 in translesion synthesis.

29 ged DNA in a process commonly referred to as translesion synthesis.

30 eta, however, led to a synergistic effect on translesion synthesis.

31 ions to the polymerase active site that slow translesion synthesis.

32 of double-strand breaks (DSBs) and performs translesion synthesis.

33 base-substitution fidelity, and abasic-site translesion synthesis.

34 oleta to positively regulate its activity in translesion synthesis.

35 witch between replication, proofreading, and translesion synthesis.

36 loping novel cancer therapeutics to suppress translesion synthesis.

37 in a potentially mutagenic process known as translesion synthesis.

38 is a PCNA-interacting protein implicated in translesion synthesis, a DNA damage tolerance process th

39 tion (E664K) within this region that enables translesion synthesis across a template abasic site or a

40 NA synthesis during base-excision repair and translesion synthesis across a wide range of chemically

41 ases, the poxviral holoenzyme cannot perform translesion synthesis across an abasic site.

42 ound to be equally important for error-prone translesion synthesis across from AAF-dG DNA adducts in

43 is required in a lesion-specific manner for translesion synthesis and base damage-induced mutagenesi

44 ons for the accuracy of DNA synthesis during translesion synthesis and for the process of Pol exchang

45 anaemia pathway, which promote ICL incision, translesion synthesis and homologous recombination (revi

46 CHN cells to dacomitinib by the loss of both translesion synthesis and homologous recombination pathw

47 B-family DNA polymerase that specializes in translesion synthesis and is essential for normal embryo

48 PDE-induced mutagenesis, we examined in vivo translesion synthesis and mutagenesis in yeast cells of

49 Therefore, translesion synthesis and mutagenesis of 1,N(6)-ethenoad

50 he Polzeta pathway is generally required for translesion synthesis and mutagenesis of the (+)- and (-

51 In this mutant strain, whereas translesion synthesis and mutagenesis of UV radiation we

52 pe as the single rev3 mutant with respect to translesion synthesis and mutagenesis.

53 PrimPol employs both translesion synthesis and repriming mechanisms to facili

54 The DDT pathways, which involve translesion synthesis and template switching (TS), are a

55 stalled replication forks: the promotion of translesion synthesis and the reinitiation of DNA synthe

56 teins required for homologous recombination, translesion synthesis, and at least two endonucleases, M

57 d DNA oxidation, reduced REV1 expression and translesion synthesis, and elevated resistance to oxidat

58 tial activity of nucleotide excision repair, translesion synthesis, and homologous recombination mech

59 duced by a crosslink plays a crucial role in translesion synthesis, and length of the duplex surround

60 ncluding mono-ubiquitylation, which promotes translesion synthesis, and sumoylation, which inhibits r

61 omotes photoproduct excision, suppression of translesion synthesis, and the localization and activati

62 Our analysis highlights the importance of translesion synthesis as a primary function of the SOS r

63 acilitate replicative bypass of damaged DNA (translesion synthesis) as TRIP interactors.

64 This in vitro translesion synthesis assay will help in understanding t

65 line DT40 that REV1, a key regulator of DNA translesion synthesis at the replication fork, is requir

66 tolerated using either a recombination- or a translesion synthesis-based bypass mechanism.

67 Surprisingly, the frequency of translesion synthesis beyond the dC*dG-N(2)-3MeE pair wa

68 The in vitro data suggest that translesion synthesis by another Y-family DNA polymerase

69 monoubiquitylation of PCNA allows mutagenic translesion synthesis by damage-tolerant DNA polymerases

70 ) delta or epsilon, a switch occurs to allow translesion synthesis by DNA polymerase eta, followed by

71 Rad6-Rad18-dependent processes that include translesion synthesis by DNA polymerases eta and zeta an

72 Mn2+ also enhances translesion synthesis by Dpo4.

73 These results and biochemical studies of translesion synthesis by mouse Pol eta indicate that Pol

74 that enzymatic switching involving localized translesion synthesis by Pol eta and mismatch excision a

75 ver, this checkpoint clamp did not stimulate translesion synthesis by Pol zeta or by DNA polymerase d

76 pair capacity of the cell has been exceeded, translesion synthesis by polymerase V (Pol V) allows DNA

77 covery and cell survival become dependent on translesion synthesis by polymerase V.

78 To better understand the mechanism of translesion synthesis by the yeast DNA polymerase eta (y

79 Blockage of translesion synthesis by these DE adducts is consistent

80 erases adhere to this bypass mechanism, then translesion synthesis by these error-prone enzymes is li

81 Translesion synthesis came at the expense of lesion-skip

82 ir is generally considered to be error free, translesion synthesis can result in mutations, making it

83 In contrast, during translesion synthesis catalyzed by pol eta or pol kappa

84 to induce three-base deletions was used for translesion synthesis catalyzed by the exo(-) Klenow fra

85 o better understand the mechanistic basis of translesion synthesis contributing to cisplatin resistan

86 Translesion synthesis depends on the trigger loop and br

87 replication, and the polymerase eta (Poleta) translesion synthesis DNA polymerase additionally promot

88 entional role for PrimPol as a mitochondrial translesion synthesis DNA polymerase for oxidative DNA d

89 tly discovered DNA-dependent DNA primase and translesion synthesis DNA polymerase found in the nucleu

90 of functional DNA polymerase (Pol) eta, the translesion synthesis DNA polymerase that readily insert

91 Polymerase eta (Poleta) is a low fidelity translesion synthesis DNA polymerase that rescues damage

92 was no involvement, however, for the Pol eta translesion synthesis DNA polymerase, the Mms2-Ubc13 pos

93 of the lesion, and bypass of the damage by a translesion synthesis DNA polymerase.

94 Translesion synthesis DNA polymerases contribute to DNA

95 belonging to the DinB class of the Y-family translesion synthesis DNA polymerases have a preference

96 uman cells, revealed the roles of individual translesion synthesis DNA polymerases in bypassing these

97 Rev1 is unique among translesion synthesis DNA polymerases in employing a pro

98 The relative roles of the yeast translesion synthesis DNA polymerases Pol zeta and Pol e

99 n vitro replication in the presence of human translesion synthesis DNA polymerases.

100 NA specifically activates two key enzymes in translesion synthesis: DNA polymerase eta, the yeast Xer

101 1) yeast, which depended highly on the known translesion synthesis enzymes Rev1 and DNA polymerase ze

102 dbrain development: neural migration and DNA translesion synthesis, essential for the replication of

103 Qualitative translesion synthesis experiments showed that pol II exo

104 nse, including the direct processing of DNA, translesion synthesis, homologous recombination, and cel

105 To examine the role of translesion synthesis in ICL repair, we generated a defi

106 Current models suggest that translesion synthesis in mammalian cells is achieved in

107 DNA damage-induced checkpoint activation and translesion synthesis in mammalian cells.

108 Analysis of translesion synthesis in repair-deficient cells revealed

109 clobutane pyrimidine dimer or abasic site by translesion synthesis in the absence of specialized tran

110 of human Y-family DNA polymerases to perform translesion synthesis in the presence of DNA-distorting

111 The involvement of translesion synthesis in this pathway has been postulate

112 Effective translesion synthesis in vertebrates requires the scaffo

113 merase V was responsible for the error-prone translesion synthesis in vivo.

114 n, nucleotide excision repair, and mutagenic translesion synthesis, in response to genotoxic insults.

115 Here we show, however, that pol-V-catalysed translesion synthesis, in the presence or absence of the

116 Translesion synthesis is a DNA damage tolerance mechanis

117 Translesion synthesis is a fundamental biological proces

118 Translesion synthesis is an essential cell survival stra

119 y incising on both sides of the ICL and then translesion synthesis is conducted across the "half-exci

120 Moreover, translesion synthesis is enhanced by altered partitionin

121 This explains why translesion synthesis is permitted without proofreading

122 site-containing DNA substrates and find that translesion synthesis is template directed with the abas

123 crosslink sites and for interaction with the translesion synthesis machinery.

124 -family polymerases that facilitate accurate translesion synthesis may promote accurate microsatellit

125 ) mutagenesis pathway is a major error-prone translesion synthesis mechanism requiring Polzeta and Re

126 e tolerance, employed in both re-priming and translesion synthesis mechanisms to bypass nuclear and m

127 When translesion synthesis occurred, epsilonA-->T mutations i

128 PCNA also stimulated translesion synthesis of a model abasic site by Pol zeta

129 These results suggest that translesion synthesis of AAF-dG adducts by Polzeta is st

130 We have analyzed the role of Rev1 in translesion synthesis of an acetylaminofluorene (AAF)-dG

131 d the role of DNA polymerase eta (Poleta) in translesion synthesis of AP sites by replicating a plasm

132 hese results show that Poleta is involved in translesion synthesis of AP sites in yeast cells, and su

133 sumed to be mutagenic because of error-prone translesion synthesis of cisplatin adducts in DNA.

134 Translesion synthesis of G-AF is achieved with high-fide

135 ic results, we present mechanistic models of translesion synthesis of these two DNA adducts, involvin

136 In particular, translesion synthesis of UV damage-containing DNA is dra

137 her critical DNA processing events including translesion synthesis, Okazaki fragment maturation and D

138 pairing; pol iota may play a limited role in translesion synthesis on bulky N2-G adducts in cells.

139 matic properties: it is less able to perform translesion synthesis on templates containing base lesio

140 n addition, PolDom can perform non-mutagenic translesion synthesis on termini containing modified bas

141 Klenow fragment (DNA polymerase I) performs translesion synthesis on this model substrate.

142 tion when either incorporating 8-oxo-dGTP or translesion synthesis opposite 8-oxo-dG.

143 Y-family hpol eta is known for translesion synthesis opposite the UV-induced DNA lesion

144 silon, to post-replicative processes such as translesion synthesis or post-replicative repair.

145 corporation of T for template G and accurate translesion synthesis past a 5S-thymine glycol (5S-Tg).

146 particularly adept at efficient and accurate translesion synthesis past a 5S-thymine glycol.

147 d all four nucleotides and catalyzed limited translesion synthesis past BaP DE-dG adducts but not pas

148 reproductive organs and are associated with translesion synthesis past bulky DNA adducts.

149 ymerases plays crucial roles in carrying out translesion synthesis past damaged bases in DNA.

150 mily DNA polymerase paralogs that facilitate translesion synthesis past damaged DNA.

151 ppressor genes and are thought to arise from translesion synthesis past deaminated cyclobutane pyrimi

152 ol) iota has been proposed to be involved in translesion synthesis past minor groove DNA adducts via

153 We evaluated the role of polymerase eta in translesion synthesis past platinum adducts by determini

154 hat polymerase eta is involved in error-free translesion synthesis past some cisplatin adducts.

155 rest, suggesting that pol eta is involved in translesion synthesis past these replication-blocking ad

156 ta support a model in which pol eta-mediated translesion synthesis past this adduct is error-free in

157 Furthermore, POLN can perform translesion synthesis past thymine glycol, a common endo

158 Y-family of DNA polymerases and facilitates translesion synthesis past UV damage.

159 bf4 kinase associates with components of the translesion synthesis pathway and that this interaction

160 eins are essential components of a mutagenic translesion synthesis pathway in Escherichia coli design

161 y, replicative pol delta and the error-prone translesion synthesis pol zeta were able to accurately b

162 Translesion synthesis polymerase eta (eta) also extends

163 PrimPol, the translesion synthesis polymerase identified inside mamma

164 icase Twinkle and the proposed mitochondrial translesion synthesis polymerase PrimPol to study lesion

165 DNA damage bypass by the translesion synthesis polymerase Rev1 is enhanced by the

166 e absence of polymerase kappa or iota, other translesion synthesis polymerase(s) could incorporate nu

167 naturally in eukaryotic Pol zeta (a family-B translesion synthesis polymerase).

168 Yeast polymerase eta, a prototypical translesion synthesis polymerase, binds both PCNA and Re

169 of Ubc13 in controlling the activity of the translesion synthesis polymerase, Rev1.

170 dies for the lesion-bearing substrate with a translesion synthesis polymerase, yeast polymerase eta.

171 me-replicating category or is an error-prone translesion synthesis polymerase.

172 Translesion synthesis polymerases (TLS Pols) are require

173 uggesting the mutual involvement of multiple translesion synthesis polymerases in bypassing the lesio

174 plicative polymerases but can be bypassed by translesion synthesis polymerases in the nucleus.

175 gated to the C5 position of thymine by human translesion synthesis polymerases leads to large numbers

176 bditis elegans and supports a model in which translesion synthesis polymerases perform a slippage and

177 recombination-associated DNA synthesis, with translesion synthesis polymerases providing a supportive

178 We report here that of two translesion synthesis polymerases tested, only DNA polym

179 sion synthesis in the absence of specialized translesion synthesis polymerases.

180 s, or how the latter process is modulated by translesion synthesis polymerases.

181 While monoubiquitination activates mutagenic translesion synthesis, polyubiquitination activates an e

182 anding the basic mechanism of a postincision translesion synthesis process in ICL repair.

183 erase but has little, if any, bearing on the translesion synthesis properties of the enzyme.

184 is dramatically stimulated by PCNA such that translesion synthesis rates are comparable with replicat

185 anconi anemia, nonhomologous end joining, or translesion synthesis repair pathways did not sensitize

186 ol becomes more promutagenic, has an altered translesion synthesis spectrum and is capable of faithfu

187 f the multi-protein complex that carries out translesion synthesis, the error-prone replication of da

188 that Rev1 plays a non-catalytic function in translesion synthesis, the role of its dCMP transferase

189 NHEJ) (yku70), mismatch repair (MMR) (pms1), translesion synthesis (TLS) (rev3), and checkpoints (mec

190 olymerase (Pol) eta in the insertion step of translesion synthesis (TLS) across the (5'S) diastereome

191 ty to copy damaged DNA in a process known as translesion synthesis (TLS) and by their low fidelity on

192 rase zeta (Pol zeta) plays a key role in DNA translesion synthesis (TLS) and mutagenesis in eukaryote

193 te unrepaired lesions: potentially mutagenic translesion synthesis (TLS) and nonmutagenic damage avoi

194 ding-deficient family A enzyme implicated in translesion synthesis (TLS) and perhaps in somatic hyper

195 om both nucleotide excision repair (NER) and translesion synthesis (TLS) and predominates during the

196 18 governs at least two distinct mechanisms: translesion synthesis (TLS) and template switching (TS)-

197 r as to which of the lesion bypass processes-translesion synthesis (TLS) and/or template switching-de

198 mediated damage avoidance and Rad18-mediated translesion synthesis (TLS) are two forms of PRR.

199 d mutagenesis through its additional role in translesion synthesis (TLS) as a subunit of DNA polymera

200 Among several hypotheses to explain how translesion synthesis (TLS) by DNA polymerase eta (pol e

201 Rad6-Rad18-dependent lesion bypass involves translesion synthesis (TLS) by DNA polymerases eta or ze

202 ponent of Pol delta, it is also required for translesion synthesis (TLS) by Pol zeta.

203 e Rad6-Rad18-dependent pathways that include translesion synthesis (TLS) by Pol(eta) or -zeta and an

204 Translesion synthesis (TLS) by Y-family DNA polymerases

205 Translesion synthesis (TLS) by Y-family DNA polymerases

206 Both the POLH-1 (pol eta) translesion synthesis (TLS) DNA polymerase and the GEI-1

207 Rev1 is a Y-family translesion synthesis (TLS) DNA polymerase involved in b

208 The Polzeta translesion synthesis (TLS) DNA polymerase is responsibl

209 ave investigated mechanisms that recruit the translesion synthesis (TLS) DNA polymerase Polkappa to s

210 Here we examine in human cells the roles of translesion synthesis (TLS) DNA polymerases (Pols) in pr

211 Here, we examine in human cells the roles of translesion synthesis (TLS) DNA polymerases (Pols) in th

212 Translesion synthesis (TLS) DNA polymerases (Pols) promo

213 Here we identify the translesion synthesis (TLS) DNA polymerases (Pols) requi

214 ys a crucial role in promoting the access of translesion synthesis (TLS) DNA polymerases (Pols) to PC

215 sions occurs by the sequential action of two translesion synthesis (TLS) DNA polymerases (Pols), in w

216 nding domains (UBDs) have been identified in translesion synthesis (TLS) DNA polymerases and it has b

217 Instead, translesion synthesis (TLS) DNA polymerases are employed

218 The roles of translesion synthesis (TLS) DNA polymerases in bypassing

219 Error-prone mechanisms rely on specialized translesion synthesis (TLS) DNA polymerases that directl

220 o its previously proposed role in recruiting translesion synthesis (TLS) DNA polymerases to gaps enco

221 ments in the isogenic cells where individual translesion synthesis (TLS) DNA polymerases were deplete

222 This review focuses on eukaryotic translesion synthesis (TLS) DNA polymerases, and the emp

223 Unique among translesion synthesis (TLS) DNA polymerases, pol zeta is

224 However, translesion synthesis (TLS) DNA polymerases, such as Rev

225 polymerases known to bypass DNA lesions: the translesion synthesis (TLS) DNA polymerases.

226 nous carcinogens using a set of low-fidelity translesion synthesis (TLS) DNA polymerases.

227 In contrast, translesion synthesis (TLS) DNAPs are suitable for repli

228 Translesion synthesis (TLS) employs low fidelity polymer

229 Translesion synthesis (TLS) employs specialized DNA poly

230 reference for using recombination (REC) over translesion synthesis (TLS) for handling H2O2-induced DN

231 Here we identify a role of poltheta in translesion synthesis (TLS) in human cells.

232 DNA translesion synthesis (TLS) is a crucial damage toleranc

233 Translesion synthesis (TLS) is a pathway in which specia

234 Translesion synthesis (TLS) is a potentially mutagenic m

235 from an origin of replication, we show that translesion synthesis (TLS) makes a prominent contributi

236 ub1 normally functions to promote error-free translesion synthesis (TLS) mediated by DNA polymerase e

237 or, PCNA, as a safeguard against error-prone translesion synthesis (TLS) of DNA.

238 t lysine 164 during polymerase eta-dependent translesion synthesis (TLS) of site-specific cis-syn cyc

239 possibly mediated by its ability to catalyze translesion synthesis (TLS) of these lesions.

240 A polymerase zeta is absolutely required for translesion synthesis (TLS) of this lesion, while loss o

241 ional specificity and the genetic control of translesion synthesis (TLS) opposite an AP site in yeast

242 Post-replication repair involves either translesion synthesis (TLS) or damage avoidance via temp

243 pathways of ICLs exist in humans that share translesion synthesis (TLS) past a partially processed I

244 polymerases that are thought to function in translesion synthesis (TLS) past different types of DNA

245 itment of damage-tolerant polymerases in the translesion synthesis (TLS) pathway of DNA damage avoida

246 ts with and regulates several members of the translesion synthesis (TLS) pathway, a DNA damage tolera

247 repair (NER), recombination repair (RR), and translesion synthesis (TLS) pathways, with substantially

248 DNA polymerase (Pol) and a more specialized translesion synthesis (TLS) Pol to overcome the obstacle

249 However, E. coli contains translesion synthesis (TLS) Pols II, IV, and V that also

250 Here we analyzed the roles of translesion synthesis (TLS) Pols in the replication of 3

251 is indispensable for promoting the access of translesion synthesis (TLS) polymerases (Pols) to PCNA.

252 switches, indicative of MMBIR, are driven by translesion synthesis (TLS) polymerases Polzeta and Rev1

253 ic consequences associated with fork demise, translesion synthesis (TLS) polymerases such as poleta p

254 In addition to translesion synthesis (TLS) polymerases, most eukaryotic

255 ty, replicative polymerases and low fidelity translesion synthesis (TLS) polymerases.

256 s, followed by bypass of the unhooked ICL by translesion synthesis (TLS) polymerases.

257 n the bypass of DNA damage, a process called translesion synthesis (TLS) that alleviates replication

258 ce that Pol II has an intrinsic capacity for translesion synthesis (TLS) that enables bypass of the C

259 ein of Saccharomyces cerevisiae functions in translesion synthesis (TLS) together with DNA polymerase

260 Consistent with activation of translesion synthesis (TLS) under these conditions, SAHA

261 polymerase-DNA minor groove interactions on translesion synthesis (TLS) was examined in vitro using

262 ll's reliance on the potentially error-prone translesion synthesis (TLS), and an error-free, template

263 sting that nucleotide excision repair (NER), translesion synthesis (TLS), and recombination each play

264 of interstrand cross-links (ICLs) involving translesion synthesis (TLS), biochemical support for thi

265 esizing past DNA lesions in a process called translesion synthesis (TLS), but how TLS polymerases gai

266 repair requires the concerted activities of translesion synthesis (TLS), Fanconi anemia (FA), and ho

267 The DNA synthesis across DNA lesions, termed translesion synthesis (TLS), is a complex process influe

268 The cellular DNA repair pathway, translesion synthesis (TLS), is disrupted by BPLF1, whic

269 A-damage processing defects are reported for translesion synthesis (TLS), non-homologous end joining

270 Three modes of DDT have been documented: translesion synthesis (TLS), template switching (TS), an

271 ice deficient for Rev1, a core factor in DNA translesion synthesis (TLS), the postreplicative bypass

272 replication of damaged genomes by promoting translesion synthesis (TLS), this comes at a cost of pot

273 by the ubiquitin ligase (E3) yRad18 promotes translesion synthesis (TLS), whereas the lysine-63-linke

274 This constitutes one of the initial steps in translesion synthesis (TLS)--a critical pathway for cell

275 with stalled replication forks and promoting translesion synthesis (TLS).

276 romoting replication although DNA lesions by translesion synthesis (TLS).

277 merases in the DNA damage tolerance pathway, translesion synthesis (TLS).

278 e involved in the tolerance of DNA damage by translesion synthesis (TLS).

279 ination (HR), nonhomologous end joining, and translesion synthesis (TLS).

280 atalyzes proficient bypass of damaged DNA in translesion synthesis (TLS).

281 therwise stall replication--a process termed translesion synthesis (TLS).

282 tive bypass of DNA lesions, a process called translesion synthesis (TLS).

283 is the large increase in mutations caused by translesion synthesis (TLS).

284 A polymerase (pol) eta, which is involved in translesion synthesis (TLS).

285 ring replication, but is believed to inhibit translesion synthesis (TLS).

286 ivation of pol V for DNA synthesis including translesion synthesis (TLS).

287 ble to assist pol delta in 8-oxo-G bypass by translesion synthesis (TLS).

288 atic relationship between the FA pathway and translesion synthesis (TLS, a post-replication DNA repai

289 st chemically defined template base lesions (translesion synthesis; TLS).

290 The contribution of translesion synthesis to survival was minor compared to

291 Biochemical assays of translesion synthesis using m6G lesion-containing templa

292 Translesion synthesis was reduced by approximately 26-37

293 on, but only Pol eta, an enzyme efficient in translesion synthesis, was able to fully bypass the addu

294 ing of how this substitution interferes with translesion synthesis, we have determined the X-ray crys

295 e the relevance of its catalytic function in translesion synthesis, we separated the Rev1 dCMP transf

296 normal DNA with high efficiency yet conduct translesion synthesis when needed.

297 duced lesions are bypassed predominantly via translesion synthesis, whereas the error-free pathway fu

298 o the G2 phase, cells utilize REV3-dependent translesion synthesis, which requires a MEC1-dependent d

299 n that can facilitate both high fidelity and translesion synthesis within the replisome during DNA re

300 help cells tolerate DNA damage by performing translesion synthesis, yet they also can be highly error