ライフサイエンスコーパス: template switching

1 ation-based mechanism (which we term "faulty template switching").

2 tly at the ends of the templates (end-to-end template switching).

3 triggers a recombinogenic process involving template switching.

4 break repair by nonhomologous end-joining or template switching.

5 replication through the DNA lesion occurs by template switching.

6 rm FoSTeS, for replication Fork Stalling and Template Switching.

7 endent pathway which presumably operates via template switching.

8 uced replication with multiple cycles of DNA template switching.

9 e via a replicative repair process involving template switching.

10 veral substitutions increased the rate of RT template switching.

11 y dimer of human telomerase does not require template switching.

12 y because of the increased opportunities for template switching.

13 n a 1.8-fold increase in the frequency of RT template switching.

14 nitiated when DNA polymerases stall, such as template switching.

15 hus supporting the hypothesis of survival by template switching.

16 nascent DNA with acceptor template promotes template switching.

17 mer strand complementarity on recombinogenic template switching.

18 y, which determines the frequency of in vivo template switching.

19 the frequency of reverse transcriptase (RT) template switching.

20 was essential for the increased frequency of template switching.

21 rred far more frequently than intermolecular template switching.

22 hydroxyurea treatment on the frequencies of template switching.

23 NA degradation influence the frequency of RT template switching.

24 at were capable of undergoing intermolecular template switching.

25 minimizing artifactual exon recombination by template switching.

26 m for analysis of reverse transcriptase (RT) template switching.

27 mologous template sequences 3' of RT promote template switching.

28 merization rate, may affect the frequency of template switching.

29 APOBEC3F, APOBEC3G, and APOBEC3H affected RT template switching.

30 template is necessary but not sufficient for template switching.

31 mall RNAs that combines chemical capping and template switching.

32 consistent with the DNA replication-related template switching.

33 ecA-independent suppression of DNA crossover template switching.

34 ynthesis and subsequent bypass by error-free template switching.

35 lusive in mammals, enabling damage bypass by template switching.

36 repair mechanisms, including mutagenesis and template switching.

37 and short overlaps between templates support template switching.

38 ication, was not appended due to inefficient template switching.

39 ing translesion DNA synthesis as well as DNA template switching.

40 ation events, and a replication error called template switching.

41 sion synthesis (TLS) or damage avoidance via template switching.

42 EJ or a replication-coupled process, such as template switching.

43 sting than an APOBEC3 "road-block" can force template switching.

44 Some gap filling occurs via template switching, a process that generates recombinati

45 t a single K63-junction supports substantial template switching activity, irrespective of its attachm

46 uss the possible biological functions of the template-switching activity of group II intron- and othe

47 The procedure exploits the template-switching activity of reverse transcriptase to

48 ile ssDNA-seq method, which exploits a novel template-switching activity of thermostable group II int

49 on-template-directed nucleotide addition and template switching allow DNA polymerases to overcome bre

50 Interestingly, template switching also provides an elegant explanation

51 These results suggest that template switching among repeated genes is a potent driv

52 ties is an important determinant of HIV-1 RT template switching and establish that HIV-1 recombinatio

53 chain termination but function by promoting template switching and formation of defective viral geno

54 R associated with 53BP1 deficiency manifests template switching and large deletions, underscoring ano

55 viral drugs can increase the frequency of RT template switching and may influence the rate of retrovi

56 ses of RTs can play different roles, such as template switching and mobility in group II introns, spa

57 ggesting that a combined mechanism involving template switching and non-homologous repair mediates th

58 , we studied the in vitro enzyme kinetics of template switching and non-template-directed nucleotide

59 e programmed sequence of events that include template switching and primer processing.

60 he yeast Rad5 protein can promote error-free template switching and replication past a DNA lesion via

61 pathways include translesion DNA synthesis, template switching and repriming.

62 n homologous sequences increases the rate of template switching and suggest that duplex formation bet

63 g is much more efficient than intermolecular template switching and that direct repeat deletions occu

64 ne a specific class of mutagen that promotes template-switching and acts by stalling replication rath

65 ol I and T4 DNA polymerase indicate that the template-switching and/or strand-displacement activities

66 eries of steps that include fork regression, template switching, and fork restoration often has been

67 rom pseudogenes, segmental duplications, and template switching, and outputs both PTES and canonical

68 s broadly include translesion DNA synthesis, template switching, and replication fork repriming.

69 inc finger domain increased the frequency of template switching approximately twofold.

70 genome rearrangements arising from frequent template switching are averted.

71 ssified as products of reverse transcriptase template switching are both enriched in platelets and re

72 The sequence requirements for template switching are compared to those for transposon

73 switching process, nontemplated addition and template switching are concurrent and competing processe

74 We found that the rate and amplitude of template switching are optimal from starter duplexes wit

75 ndividually produced lentiviruses eliminated template-switching artefacts and enhanced the performanc

76 n in cultured cells using vectors that force template switching at defined locations.

77 Template switching at inverted repeats during DNA replic

78 a DNA repair pathway initiated by polymerase template switching at microhomology, which can produce t

79 n (MMBIR), a replicative mechanism involving template switching at positions of microhomology.

80 l in which dysregulated Rad5 causes aberrant template switching at replication forks.

81 ediates produced by RecA or RecA-independent template switching at stalled forks or postreplication g

82 hat arise by nascent strand misalignment and template-switching at the site of short repetitive seque

83 By employing a template-switching-based sequencing protocol, Nano3P-seq

84 Template switching between copackaged human immunodefici

85 Retroviral recombinants result from template switching between copackaged viral genomes.

86 We examined BIR and template switching between highly diverged sequences in

87 Frequency and distribution of template switching between homologous donor and acceptor

88 elongation phase characterised by extensive template switching between homologous, homeologous and m

89 ropriately active Exo1 may facilitate faulty template switching between nearby inverted repeats to fo

90 cond-strand transfer rather than from forced template switching between RNAs.

91 eat Amplification (ODIRA) which results from template switching between the leading and lagging stran

92 Finally, we show that template switching between the tRNA and the plasmid tran

93 rse transcriptase synthesizes cDNA dimers by template switching between two tRNA templates and initia

94 el for retroviral transduction suggests that template switching between viral RNAs and polyadenylatio

95 products, including some that resulted from template switching between virus and host sequences, wer

96 ecombination occurs solely by intermolecular template switching (between copackaged RNAs), deletions

97 his study, we present a detailed analysis of template switching biases with respect to the RNA templa

98 t results from more efficient suppression of template switching by 3' exonucleases targeted to the la

99 e input mutant RNA3 3' UTR due to end-to-end template switching by BMV replicase during (-)-strand sy

100 the enzyme-dependent factors that influence template switching by comparing the RTs from human immun

101 The biochemical mechanism of template switching by human immunodeficiency virus type

102 n and integration occurred due to end-to-end template switching by mammalian RNA polymerase II (RNAP

103 The tested hypothesis is that template switching by reverse transcriptase is promoted

104 dependent RNA polymerase (RdRp), followed by template switching by the RdRp and continued RNA synthes

105 stems indicate that recombination occurs via template switching by the virus-encoded RNA-dependent RN

106 (H539N, D549N) decreased the frequency of RT template switching by twofold.

107 he RNase H domain decreased the frequency of template switching by twofold.

108 letion of template end-to-end transposition (template switching) by RNA polymerase II, respectively.

109 ma of RNA gene evolution and demonstrate how template switching can both create perfect stems with a

110 Template switching can occur during the reverse transcri

111 Template switching causes crossovers in areas of sequenc

112 Following a template-switching cDNA amplification protocol, seven cD

113 r is local, polarity sensitive, and prone to template switching, characteristics that are consistent

114 ion initiates serial, microhomology-mediated template switching (chromoanasynthesis) that produces lo

115 erve of genetic information and suggest that template switching contributes to HIV-1 genomic integrit

116 plication occurs by translesion synthesis or template switching (copy choice) when a duplex molecule

117 ndent and -independent RNase H activities in template switching could be determined.

118 processes-translesion synthesis (TLS) and/or template switching-depend on the activation of the repli

119 Full hairpin bypass often involves template-switching DNA synthesis, subsequent realignment

120 ternally placed RNA-dependent RNA polymerase template-switching donor signal, discontinuous transcrip

121 ion, all of which contain potential internal template-switching donor signals, can function to increa

122 xclude the occurrence of mixed infection and template switching during amplification, laboratory arti

123 rather, NOH-1S appears to be an artifact of template switching during cDNA synthesis.

124 d region, which could promote intramolecular template switching during cDNA synthesis.

125 To determine the relative rates of RT template switching during copying of RNA and DNA templat

126 s, and many mutations have the signatures of template switching during DNA repair synthesis.

127 Our study reveals that template switching during DNA replication is a prevalent

128 complex breakpoint patterns consistent with template switching during DNA replication or repair, and

129 epeat expansions could occur upon fortuitous template switching during DNA replication.

130 reduced dNTP binding RT mutants can promote template switching during minus strand synthesis more ef

131 eterologous residues resulting from apparent template switching during negative-strand synthesis of s

132 rom deep sequencing due to artifacts such as template switching during PCR amplification.

133 ng appears to be a conserved requirement for template switching during plus-strand DNA synthesis of H

134 apsid particle so that it supports efficient template switching during plus-strand DNA synthesis.

135 l for large-scale repeat expansions based on template switching during replication fork progression t

136 We devised a generalized mutation model of template switching during replication that extends exist

137 Template switching during reverse transcription contribu

138 tion is inherently error prone due to random template switching during reverse transcription of RNA t

139 Template switching during reverse transcription promotes

140 viruses is a multistep process that requires template switching during reverse transcription.

141 ctors indicated that the in vivo rates of RT template switching during RNA- and DNA-dependent DNA syn

142 The relative rates of in vivo RT template switching during RNA- and DNA-dependent DNA syn

143 tegies provided information on the impact of template switching during RNA-directed transcription.

144 ng antisense RNA (aRNA) amplification with a template-switching effect (Clonetech, Palo Alto, CA).

145 AMHD1 degradation by Vpx did not alter HIV-1 template switching efficiency in activated CD4(+) T cell

146 ellular dNTP concentrations, decreased HIV-1 template switching efficiency in macrophages to the leve

147 ase H activity, supporting that the elevated template switching efficiency of the mutants was not the

148 In this study, we first observed that HIV-1 template switching efficiency was nearly doubled in huma

149 of the dNTP concentrations influences HIV-1 template switching efficiency, particularly in macrophag

150 that the presence of a 5'-m(7)G cap enhances template switching efficiency.

151 nontemplated additions did little to improve template switching efficiency.

152 ap as a key structural element for enhancing template switching efficiency.

153 THP-1 cells have a 2-fold increase in HIV-1 template switching efficiency.

154 ed on hybrid RNA-DNA reverse splicing and on template switching errors by reverse transcriptase.

155 haplotyping do not suffer from mispriming or template-switching errors.

156 sed fork, and facilitate a Fork Stalling and Template Switching event producing the complex rearrange

157 se genetics system, we demonstrated that the template-switching event during intergenic region (IR) s

158 RT template switching events could occur during either RNA-

159 The RdRp-driven template switching events occurred between either identi

160 e involved in replicase "landing" during the template switching events.

161 tions occur primarily through intramolecular template switching events.

162 may be a hot spot for reverse transcriptase template switching events.

163 nsertion cycles (TIC), likely resulting from template switching events.

164 priate recombination that could occur during template switching events.

165 We hypothesized that intermolecular template-switching events (recombination) occurred at a

166 These microinsertions are consistent with template-switching events and suggest a particular spati

167 Template-switching events during reverse transcription a

168 g, we developed an in vivo assay in which RT template-switching events during viral replication resul

169 requency of recombinants containing multiple template-switching events is higher than expected.

170 rrupted terminal duplications accompanied by template-switching events.

171 However, Psi did not increase the rate of template switching for shorter direct repeats.

172 DNA replication model of 'fork stalling and template switching' for CNV formation, we hypothesized t

173 ication-based, for example fork stalling and template switching (FoSTeS) and microhomology-mediated b

174 nduced Replication (MMBIR)/Fork Stalling and Template Switching (FoSTeS) as a mechanism of their form

175 ication-based mechanism of fork stalling and template switching (FoSTeS) to explain the complex genom

176 logous end joining (NHEJ), fork stalling and template switching (FoSTeS), and microhomology-mediated

177 nts with the most significant alterations in template switching frequencies was similar to that of th

178 Q151N, and M184I) dramatically increased RT template-switching frequencies by two- to sixfold in a s

179 Since alterations to the RT template switching frequency can result in insertions or

180 as the dNTP concentration was decreased, the template switching frequency progressively increased for

181 nces generated with hydroxyurea, we examined template switching frequency using a lacZ-based tandem r

182 independent RNase H did not restore the high template switching frequency, indicating that polymerase

183 The double mutants exhibited low template switching frequency, indicating that the RNase

184 everse transcriptase (RT) that influence its template-switching frequency are not known.

185 re was introduced into the template RNA, the template-switching frequency increased 5-fold for wild-t

186 ther analyses showed that the intermolecular template-switching frequency was unaffected by the seque

187 A model termed Fork Stalling and Template Switching has been proposed previously to expla

188 igonucleotide and the reaction conditions on template switching have been explored.

189 ve-strand synthesis, genome replication, and template switching; (ii) a full-length SIN RNA carrying

190 via multiple rounds of strand invasion with template switching in mouse.

191 ot most, of these events are associated with template switching in postreplication gaps as opposed to

192 lating the choice between TLS and error-free template switching in replicative DNA damage bypass.

193 zinc finger domain to study its effect on RT template switching in vivo and to explore the role of NC

194 activities during reverse transcription and template switching in vivo have not been determined.

195 his interaction promotes fork remodeling and template switching in vivo was unknown.

196 b 3'-coterminal SIN RNA fragment and undergo template switching in vivo.

197 several recombinants that were generated by template switching involving internal positions in the R

198 lling is driven in S-phase by UBC13-mediated template switching involving REV1 and the TLS polymerase

199 Template switching is a DNA damage bypass pathway in whi

200 Template switching is a DNA-replication-related mutation

201 DNA replication-related template switching is a mutation mechanism that creates

202 Template switching is believed to happen in a sequential

203 these analyses indicate that intramolecular template switching is much more efficient than intermole

204 on junctions are infrequent, suggesting that template switching is not intrinsically mutagenic.

205 Template switching is required during normal retroviral

206 ides of the crossover point, suggesting that template switching is the most likely model for the mech

207 Template switching is typically thought to trigger large

208 For template switching, kinetic analysis revealed that the t

209 which we demonstrate proof-of-concept for a 'template-switching' lentiviral vector that harnesses rec

210 mbination junction and that the triggers for template switching may be sequence independent.

211 Here, we tested the hypothesis that template switching may instead contribute to replication

212 rk structures containing template damage and template switching mechanism of lesion bypass reveal tha

213 lts suggest that spontaneous SCE occurs by a template switching mechanism.

214 e interviral recombinants are generated by a template-switching mechanism during RNA replication by t

215 est the previously proposed replicase-driven template-switching mechanism for recombination, a partia

216 al and direct support for a replicase-driven template-switching mechanism of RNA recombination.

217 omplex that allows bypass of DNA lesion by a template-switching mechanism.

218 Rather, the data were consistent with a template-switching mechanism.

219 e viral RNA-dependent RNA polymerase using a template-switching mechanism.

220 ependent DNA synthesis across DNA lesions by template switching mechanisms.

221 RNAs can occur by either template choice or template-switching mechanisms.

222 networks from genetic sequence data under a template switching model of recombination.

223 A replicase-driven template-switching model is presented to explain recombi

224 Due to template switching, most of the polynucleotides contain

225 ndamental questions related to proofreading, template switching, mRNA capping, and the role of the en

226 Here, we show that the template-switching mutations (TSMs) have participated in

227 evious results indicated that intramolecular template switching occurred far more frequently than int

228 It has been postulated that template switching occurs after pauses in the action of

229 serotypic recombinant genomes indicates that template switching occurs by a mechanism that may requir

230 By implying that recombinogenic template switching occurs roughly four times on average

231 alindrome-associated mutations suggests that template-switching occurs readily during chromosomal rep

232 -length homologous recombinants generated by template switching of BMV replicase with a nascent UTR f

233 This template jumping is analogous to the template switching of retroviral reverse transcriptases

234 and are likely artifacts arising from random template switching of reverse transcriptase and/or seque

235 We found that APOBEC3F could promote template switching of RT, and this was dependent on the

236 implicating in vitro artifacts generated by template switching of Taq polymerase and reverse transcr

237 e RNAs, which are thought to be generated by template switching of the viral RNA-dependent RNA polyme

238 anneal to the matching rGrGrG 3'-end of the template-switching oligo (TSO), allowing the reverse tra

239 ption that is RNA directed, but also achieve template switching on a discontinuous RNA template, and

240 proximal repeat, consistent with more common template switching on the leading strand.

241 scription, showed that hydroxyurea increased template switching only when polymerase-dependent RNase

242 s found by us cannot be easily explained via template switching owing to the combination of the short

243 n chain by Ubc13-Mms2/Rad5 routes DDT to the template switching pathway.

244 nslesion synthesis (TLS), and an error-free, template-switching pathway in Saccharomyces cerevisiae.

245 e-dependent amplification characteristics of Template-Switching PCR and validate its use for microarr

246 Template switching preferentially involves active topolo

247 or promoting replication fork regression and template switching; previously, we suggested a role for

248 contrast to the current understanding of the template switching process, nontemplated addition and te

249 We propose that template switching promoted by Brh2 provides a mechanism

250 Many scRNA-Seq approaches rely upon the template switching property of Moloney murine leukemia v

251 by Taq-induced nucleotide substitutions and template switching, provides an accurate representation

252 3'-DNA overhangs progressively decreased the template-switching rate, even when complementary to the

253 hese data suggest that reverse transcriptase template switching rates can be altered significantly wi

254 Template switching rates of Moloney murine leukemia viru

255 NA copackaging could not vary, MLV and HIV-1 template switching rates were indistinguishable.

256 This rescue is based on two sequential template-switching reactions that allow DNA replication

257 ssay in which direct repeat deletion through template switching reconstitutes a functional green fluo

258 d sequences at the donor and acceptor sites, template switching requires at least three other cis-act

259 t retroviral recombination, like strong stop template switching, requires the RNase H activity of rev

260 ase H mutations that increased and decreased template switching, respectively.

261 Template-switching reverse transcription is widely used

262 synthetically capped 5' mRNA fragments with template-switching reverse transcription.

263 on-template-directed nucleotide addition and template switching showed similar rates and were approxi

264 several of these mutations also decreased RT template switching, suggesting that they alter the predi

265 These mutations also decreased RT template switching, suggesting that they altered the bal

266 tations in the RNase H primer grip decreased template switching, suggesting that they reduced RNase H

267 eler Rdh54 as the first protein required for template switching that does not affect simple gene conv

268 by end joining or by microhomology-mediated template switching, the latter forming complex tandem du

269 In template switching, the newly synthesized sister strand

270 proteins are strongly impaired in promoting template switching, thus supporting the hypothesis of su

271 enzymatic enrichment of 5' capped RNAs with template switching to create sequencing libraries.

272 and the template strand sufficient to direct template switching to the U3/R junction.

273 ymerization, non-templated base addition and template switching together allow us to propose a revise

274 Template switching (TS) plays crucial roles in retrovira

275 rted by homologous recombination is prone to template switching (TS) that can generate deleterious ge

276 een documented: translesion synthesis (TLS), template switching (TS), and repriming.

277 ays, which involve translesion synthesis and template switching (TS), are activated by the ubiquityla

278 mechanisms: translesion synthesis (TLS) and template switching (TS)-dependent pathways.

279 e rates of intramolecular and intermolecular template switching, two spleen necrosis virus-based vect

280 utations in RT increased the frequency of RT template switching up to fivefold, while all of the muta

281 ates lacking the poly(A) tail do not support template switching; (v) full-length SIN RNAs lacking the

282 of a sequence duplication, the frequency of template switching varied more than threefold among full

283 by mediating replication fork regression and template switching via its DNA helicase activity and Rad

284 Template switching was also assayed by using transductio

285 Template switching was confirmed in vitro, where the del

286 he 701-bp direct repeat and the frequency of template switching was greater within the 5' regions in

287 e restored in both copies of the redundancy, template switching was not necessarily restored.

288 action of clones with sequence predictive of template switching was reduced when extracts deficient i

289 nts of HIV-1 RT that affect the frequency of template switching, we developed an in vivo assay in whi

290 ts of murine leukemia virus RT important for template switching, we developed an in vivo assay in whi

291 rse transcription increases the frequency of template switching, we established conditions that lengt

292 rease the frequency of reverse transcriptase template switching, we propose that an equilibrium exist

293 mine the relative magnitude and mechanism of template switching, we studied the in vitro enzyme kinet

294 on-template-directed nucleotide addition and template switching were compared to that of standard pri

295 The effects of NC mutations on RT template switching were determined by using a previously

296 e rates of intramolecular and intermolecular template switching were determined.

297 n to pause reverse transcriptase and promote template switching, were found in most in vitro crossove

298 is is expected to reduce the frequency of RT template switching, whereas annealing the nascent DNA wi

299 g, we developed an in vivo assay in which RT template switching within direct repeats functionally re

300 eletion of a short duplicated sequence or by template switching within imperfect inverted repeat (qua