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 ynthesis and subsequent bypass by error-free template switching.

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

5 repair mechanisms, including mutagenesis and template switching.

6 veral substitutions increased the rate of RT template switching.

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

8 y because of the increased opportunities for template switching.

9 and short overlaps between templates support template switching.

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

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

12 hus supporting the hypothesis of survival by template switching.

13 nascent DNA with acceptor template promotes template switching.

14 mer strand complementarity on recombinogenic template switching.

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

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

17 was essential for the increased frequency of template switching.

18 rred far more frequently than intermolecular template switching.

19 hydroxyurea treatment on the frequencies of template switching.

20 NA degradation influence the frequency of RT template switching.

21 at were capable of undergoing intermolecular template switching.

22 minimizing artifactual exon recombination by template switching.

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

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

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

26 template is necessary but not sufficient for template switching.

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

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

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

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

31 replication through the DNA lesion occurs by template switching.

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

33 endent pathway which presumably operates via template switching.

34 uced replication with multiple cycles of DNA template switching.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 Template switching between copackaged human immunodefici

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 Template switching can occur during the reverse transcri

80 Template switching causes crossovers in areas of sequenc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 Template switching during reverse transcription contribu

105 Template switching during reverse transcription promotes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

121 RT template switching events could occur during either RNA-

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

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

124 tions occur primarily through intramolecular template switching events.

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

126 priate recombination that could occur during template switching events.

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

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

129 Template-switching events during reverse transcription a

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

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

132 rrupted terminal duplications accompanied by template-switching events.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 Template switching is required during normal retroviral

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

160 For template switching, kinetic analysis revealed that the t

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

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

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

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

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

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

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

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

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

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

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

172 Due to template switching, most of the polynucleotides contain

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 Template switching rates of Moloney murine leukemia viru

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

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

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

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

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

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

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

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

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

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

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

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

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

205 In template switching, the newly synthesized sister strand

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

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

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

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

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

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

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

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

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

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

216 Template switching was also assayed by using transductio

217 Template switching was confirmed in vitro, where the del

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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