ライフサイエンスコーパス: transversion

1 e wild-type protein sequence through a codon transversion.

2 utator effect) is observed for the G.C-->T.A transversion.

3 ly 16%, and both included a dominant G --> T transversion.

4 to repair this lesion results in G:C to T:A transversion.

5 approximately fourfold that of each type of transversion.

6 -oxoG/dAMP base pair results in a G-C to T-A transversion.

7 osite template 8-oxoG can result in a G to T transversion.

8 dual coding potential that leads to G --> T transversions.

9 which results in G.C --> T.A or G.C --> C.G transversions.

10 n defects associated with most, but not all, transversions.

11 ecies, and this lesion results in G:C to T:A transversions.

12 nce of the human enzyme for T-->A over A-->T transversions.

13 which leads to AL-II-dA-->T and AL-II-dG-->T transversions.

14 (C to T and A to G) and cannot produce base transversions.

15 ication, resulting specifically in GC --> TA transversions.

16 fold more mutagenic inducing primarily G-->T transversions.

17 pposite template adenine to yield A-T to C-G transversions.

18 ments include inversions, transpositions and transversions.

19 ood patterns and so do A <--> C and G <--> T transversions.

20 s pattern, with most mutations being GC-->TA transversions.

21 gistically to minimize the levels of G --> T transversions.

22 high mutation rates, all due to G:C --> T:A transversions.

23 ns and very unusual kinds (spectrum), mainly transversions.

24 tations, with 78% of these being A:T --> T:A transversions.

25 genic inducing primarily targeted Fapy.G-->T transversions.

26 t, where both lesions induced targeted A-->C transversions.

27 n generating C --> T transitions and C --> G transversions.

28 deoxyguanosine (OxodG) gives rise to G --> T transversions.

29 ighly mutagenic, causing G --> T and G --> C transversions.

30 cy and in a significant increase in AT-to-TA transversions.

31 l systems, transitions were more common than transversions.

32 e the lesion, primarily resulting in G --> T transversions.

33 f generating C --> T transitions and C --> G transversions.

34 ates are generally extended more easily than transversions.

35 that almost all of the mutations are GC-->TA transversions.

36 mutagenic, causing almost exclusive G --> C transversions.

37 ns, all somatic APC mutations were G:C-->T:A transversions.

38 and caused a mixture of G --> T and G --> C transversions.

39 ations in the RpoB gene, 20% were Gua to Thy transversions.

40 relatively frequent, and a large decrease in transversions.

41 7 Endonuclease I preferentially corrects A/T transversions.

42 n spectrum from predominantly T-->A to T-->G transversions.

43 ypes by having a higher frequency of G:C>T:A transversions.

44 uld account for the commonly detected G to T transversions.

45 especially large relative excess of G:C>T:A transversions.

46 bited a similar context effect: 4-fold G-->T transversions (24% versus 6%) occurred in the 5'-TGT seq

47 with predominant G --> C followed by G --> T transversions, 9% deletions of 1-3 nucleotides, and 6% i

48 sitions (G to A) and an adenosine-to-uridine transversion (A to U).

49 by chronic oxidative stress including GC>TA transversions (a fingerprint of 8-oxoG:A mismatches).

50 n of A.8-oxoG mispairs results in C:G to A:T transversions, a form of genomic instability.

51 er oxidative stress condition are G:C to T:A transversions, a signature of 8-oxoguanine (8-oxoG).

52 Transversions accounted for 64% of sequence differences

53 oxR V. cholerae overexpressing TcpP, several transversions affecting nucleotides within two direct re

54 h adenine (8-oxoG:A), leading to a G:C-->T:A transversion after replication.

55 creased the individual rates of an A.T-->T.A transversion, an A.T-->G.C transition and the pooled rat

56 ent viruses through a nucleotide A200-to-T/C transversion and a vpr null mutation, but these isolates

57 ns in a lacZ reversion system, the G.C-->C.G transversion and A.T-->G.C transition are strongly enhan

58 at demethylation associated with C:G --> G:C transversion and C:G --> T:A transition mutations was ob

59 T7 RNAP indicated an increased frequency of transversion and insertion mutations compared to all T/A

60 (specific increases in relative frequency of transversion and insertion/deletion [indel] mutations).

61 t DinB(Pa) has a propensity to promote C-->A transversions and -1 frameshift mutations within poly(dG

62 ual specificity: preferential enhancement of transversions and -1 frameshifts.

63 -dA is a miscoding lesion generating A --> T transversions and A --> G transitions.

64 Indeed, C-to-G transversions and CpG transitions, which together consti

65 AT-to-CG transversions and deletions at microhomologies were enha

66 potentially contributing to A-->T and A-->C transversions and frameshift mutations observed in cells

67 eplication, specifically in the avoidance of transversions and frameshift mutations.

68 pes similar to dnaX36: strong enhancement of transversions and frameshifts and only weak enhancement

69 tions induced by the POLD1-R689W are GC-->TA transversions and GC-->AT transitions, with transversion

70 the Sod1-null mice indicated mainly GC-to-TA transversions and GC-to-AT transitions, signature mutati

71 DNA 8-oxoguanine (8-oxoG) causes transversions and is also implicated in frameshifts.

72 ere is a significant mutational bias against transversions and significant variation in rates of chan

73 A wide spectrum of transitions, transversions and single base deletions are observed.

74 tatistically significant increases in G-to-T transversions and small tandem base deletions (P = 0.007

75 framework regions, most were R mutations and transversions and transitions equally contributed.

76 particularly A to T/T to A and C to G/G to C transversions) and small insertions/deletions (in/dels).

77 ransversions involve the C at CpG sites (CpG transversions) and that their rate is comparable to the

78 Transitions were more common than transversions, and the probability of a transversion inc

79 G.C-->A.T mutations and a hotspot T.A-->G.C transversion are known to increase with the frequency of

80 nce comparisons; however, several individual transversions are more frequent than the least common tr

81 Though the spontaneous G:C to C:G transversions are rare events, the pathways leading to t

82 s and the percentage of chemotherapy-related transversions are similar in t-AML and de novo AML, indi

83 enotoxic in human cells, and that G.C to T.A transversions are the most prevalent mutations induced b

84 describe the discovery of novel C > A/G > T transversion artifacts found at low allelic fractions in

85 istent with the occurrence of A x T to T x A transversions as common mutations in animal cells treate

86 utA in mutational specificity (predominantly transversions), as well as SOS independence, but in a pu

87 don frequency, bias-favoring transition over transversion, as well as explicit phylogenetic informati

88 here that BiSeqS can be applied to evaluate transversions, as well as small insertions or deletions,

89 inucleotide (deletion T followed by a T to A transversion) associated with SLE in subjects of Europea

90 This G.C to T.A transversion at codon 249, however, has been thought to

91 In contrast, a G-to-C transversion at G+4 is lethal; RNAs carrying this mutati

92 levated Hb F levels and found a novel T-to-G transversion at nucleotide (nt) -567 of the HBG2 promote

93 Molecular analysis identified a C to G transversion at nucleotide -206 from the transcription s

94 >C transversion at nucleotide 109 predicts an amino acid ch

95 of the common BRAF missense mutation (T-->A transversion at nucleotide 1796) using restriction enzym

96 A virus with an A-->C transversion at position -3 replicates as well as wild-t

97 chromosome 17, and then ascribed to a C-->A transversion at position 3480 of the Tnf gene, correspon

98 ignature defined by a high prevalence of A>C transversions at AA dinucleotides.

99 tional signature characterized by C:G to A:T transversions at CCR sequence contexts that may have ari

100 ed by an increase in C:G-->A:T and A:T-->T:A transversions at certain mutagenic hot spots.

101 Transversions at GC base pairs in the supF gene were the

102 tably, we observed a high frequency of C-->G transversions at the cytosine residues targeted by both

103 AFB(1) frequently induces G:C to T:A transversions at the third base in codon 249 of TP53 and

104 This T to A transversion, at base 131 of the coding sequence, occurs

105 ), synonymous transitions (A(s)), synonymous transversions (B(s)), and nonsynonymous substitutions (K

106 base editing toolbox by developing cytosine transversion base editors.

107 or phenotype characterized by enhancement of transversion base substitutions and certain (-1) framesh

108 was extremely miscoding (>90%) with G --> T transversions being predominant.

109 Nine transversions between -96 to -83 reduced toxT promoter a

110 We also described the transversion bias, which is the preference for some tran

111 three different codon positions, transition/transversion biases, and codon usage.

112 s that also account for codon and transition:transversion biases.

113 nucleotide transitions are more common than transversions, by roughly a factor of two.

114 advances, a hypothetical model for the first transversion (C*G->G*C) base editor can now be proposed.

115 et extreme obesity due to a novel homozygous transversion (c.298G-->T) in LEP, leading to a change fr

116 onal-candidate genes detected a heterozygous transversion (c.386A-->T) in exon 3 of the gene for chro

117 ns approximately CpG transversions > non-CpG transversions, captures qualitative features of the muta

118 itution to a stop codon and one dinucleotide transversion compared to the donor genomic DNA.

119 caused by 8-oxodG, and the hallmark A:T->C:G transversions conformed to the known replication errors

120 iparallel Flop orientation, or with multiple transversions, conserving their base composition but cha

121 have an unexpected high frequency of A:T>T:A transversions, consistent with exposure to aristolochic

122 sitional cell cancers, and (iii) A:T --> T:A transversions dominate the p53 mutational spectrum in th

123 Transversions dominate the spectrum of spontaneous mutat

124 leomycin resistance gene and that G.C-to-T.A transversions dominated the spectrum in cells transcribi

125 otentially cause cancer by producing G --> T transversions during DNA replication.

126 cytosine, T = thymine), typically outnumber transversions (e.g., exchanges between a purine and a py

127 tations are C:G->T:A transitions or C:G->G:C transversions enriched for the APOBEC mutagenesis signat

128 ater genetic variability, with more frequent transversion events, than did populations in control and

129 anged from 3.1% to 9.8%, whereas the G --> T transversion frequencies observed upon Fapy.dG bypass we

130 ions > non-CpG transitions approximately CpG transversions > non-CpG transversions, captures qualitat

131 The C>A transversion has been identified in the heterozygous sta

132 that there is a strong coincidence of G to T transversion hotspots in lung cancers and sites of prefe

133 mosaic for a novel c.351C > G (p.Asn117Lys) transversion in ACTA2.

134 The first mutation, a T-->G transversion in codon 64, is predicted to change a conse

135 mapping and the identification of a c.504G>C transversion in ELOVL4 resulting in the p.L168F substitu

136 c causes of sickle cell disease (requiring a transversion in HBB) and Tay-Sachs disease (requiring a

137 ditional TA repeats in intron 2 and a G-to-T transversion in intron 3 that were sufficient to promote

138 A single G>C transversion in position -3 of the new Alu exon was insu

139 a deletion in HEXA); to install a protective transversion in PRNP; and to insert various tags and epi

140 on detected in LG-CMS patients is a c.*22C>A transversion in the 3'-untranslated region (UTR).

141 The method revealed an A-->T transversion in the 5' splice site of intron 2 that is t

142 chromosome 18 and then ascribed to a T to A transversion in the acceptor splice site of intron 4 at

143 nist application showed that each amino acid transversion in the beta 3-v2 subunit (P11S, S15F, and G

144 7:H7 strain ATCC 43895, a guanine-to-thymine transversion in the csgD promoter created strain 43895OR

145 PI 518671]) as a reference, a G --> T(2,822) transversion in the genomic DNA sequence at a functional

146 A cytosine to adenine transversion in the mitochondrially encoded NADH dehydro

147 could explain the high levels of G:C --> T:A transversions in cells treated with bleomycin.

148 Here we present BEs that cause C-to-A transversions in Escherichia coli and C-to-G transversio

149 mutations (one transition in exon 8 and two transversions in exons 5 and 8, respectively), one in-fr

150 cated proteins, dominant alleles all contain transversions in highly conserved amino acids of the ext

151 PAH-DNA adducts, induce predominantly G-to-T transversions in human cells.

152 Two transversions in intron 1 (T2951033A homozygote and hete

153 ozygote and heterozygote, C2951049A) and one transversions in intron 7 (G2924536C homozygote and hete

154 transversions in Escherichia coli and C-to-G transversions in mammalian cells.

155 und that transitions were more frequent than transversions in miRNAs.

156 However, the rate of AT-->CG transversions in our mutT(+) progenitor strain is some t

157 sites in vitro, and binding was abrogated by transversions in the binding sites that conserved the in

158 re was no significant increase in G:C to T:A transversions in the ogg1(-/-) clones, which would be ex

159 tational pattern is consistent with dG to dT transversions in the repetitive guanine tracts.

160 have distinct TP53 mutations, such as G to T transversions in the second guanine of codon 249 (AGG to

161 The signature mutation of G:C->T:A transversions in the treated cells accorded with the wel

162 than transversions, and the probability of a transversion increased with increasing A + T content at

163 Probability of a transversion increased with increasing A + T content of

164 n, which was restored to wild type by G to T transversion induced by oxidative stress.

165 ct responsible for the observed pattern of G transversions induced by exposure to elevated glucose or

166 s only Pol V was indispensable for the T-->A transversion introduced by these lesions.

167 ransversions, we find that the most frequent transversions involve the C at CpG sites (CpG transversi

168 The G --> T transversion is the dominant mutation induced by the cat

169 UUC, dominated by otherwise rare A:T to T:A transversions, is identical to that observed in UUC asso

170 genic in Escherichia coli, producing G --> T transversions; it thermally stabilizes the DNA duplex.

171 It can be used to detect the transversion mutation between pyrimidines and purines.

172 45G > A c.427G > A p.Ala143Thr) and an ITGB6 transversion mutation in Exon 6 (g.27415T > A c.825T > A

173 l candidate gene analyses revealed an A to T transversion mutation in exon 9 of the glucokinase gene,

174 es was found, with much more transition than transversion mutation in the D genome after its divergen

175 We report a G>T transversion mutation in the last nucleotide of exon 2,

176 In addition, as the ratio of transition and transversion mutation is often used as a discriminative

177 Transversion mutation of the HP1 loop produced a smaller

178 The average ratios of transition to transversion mutations (Ts/Tv) in diverging LTRs were >1

179 cing analysis showed an enrichment in G-to-C transversion mutations and further supports the idea tha

180 rch out rare 8-oxoguanine lesions to prevent transversion mutations arising from oxidative stress.

181 UNGs are relatively ineffective in restoring transversion mutations at C:G pairs during hypermutation

182 To identify those nucleotides a set of 27 transversion mutations in H11 was constructed and their

183 of both genes was linked to smoking-related transversion mutations in lung tumors.

184 is highly mutagenic, resulting in G:C to T:A transversion mutations in the absence of repair.

185 rease in the frequency of transition but not transversion mutations in the presence of ribavirin.

186 the frequency of Ha-ras codon 61 A(182)-->T transversion mutations in this cell population compared

187 ions should occur at a frequency of 1/15000, transversion mutations should occur at a frequency of le

188 romoter to suppress transcription, while p53 transversion mutations were most strongly associated wit

189 expression correlates with C-to-A and C-to-G transversion mutations within 5'-TC dinucleotide motifs

190 ations of the AC-GT ends of the ZRE, whereas transversion mutations within the central 5 bp of the ZR

191 eta and Rev1 together are required for G-->T transversion mutations, a major type of mutagenesis indu

192 nalysis showed enrichment of G-->A and C-->T transversion mutations, increased mutation frequency, an

193 iate base excision repair and prevent G to T transversion mutations.

194 pecific single-nucleotide polymorphism (SNP) transversion mutations.

195 mon oxidative lesions in DNA and can promote transversion mutations.

196 replication resulting in guanine to thymine transversion mutations.

197 which included a 8.7% G-->T and a 1.2% G-->C transversion mutations.

198 -2'-deoxyguanosine (OG), produces G:C to T:A transversion mutations.

199 ighly mutagenic, causing G --> C and G --> T transversion mutations.

200 tagenic, producing almost exclusively G to C transversion mutations.

201 can suppress the mutH-dependent increase in transversion mutations.

202 product, which can lead to downstream G to T transversion mutations.

203 verse transcription by enhancement of G-to-C transversion mutations.

204 error-free fashion, thus preventing GC-->AT transversion mutations.

205 mutation load as well as elevated levels of transversion mutations.

206 A novel transversion mutator phenotype was reported recently in

207 dues in RGYW motifs along with a decrease in transversions normally related to UNG2 activity.

208 The presented data show that transitions and transversions occur during HRSV replication and that the

209 NPs, accounting for 69.8% in cattle; (2) the transversion occurs most frequently (38.56%) in cattle w

210 Remarkably, a cytosine-to-guanine (C-->G) transversion occurs specifically at target cytosines, al

211 Although transversion of U8A abrogates signalling of yopQ(1-10),

212 om affected persons displayed excess somatic transversions of a guanine-cytosine pair to a thymine-ad

213 By generating transversions of every single nucleotide in yopQ(1-10),

214 m A* of adenine in DNA may result in AT-->CG transversions or AT-->GC transitions, which can eventual

215 OR, 3.37; 95% CI, 1.03-11.06), and G:C-->T:A transversions (OR, 10.53; 95% CI, 1.77-62.55) compared w

216 5% confidence interval (CI), 1.17-3.78], p53 transversions (OR, 3.37; 95% CI, 1.03-11.06), and G:C-->

217 In family B, a G-to-T transversion (ORF15+1176G>T) resulted in a nonsense muta

218 Both lesions promote G --> T transversions overall, with dG-N(2)-AAF being less mutag

219 significantly increased frequency of G --> T transversions (p < 0.0003; relative to the control), whi

220 001) and a signature mutation of G:C --> T:A transversions (p < 0.03), relative to the control.

221 y via a particular one of the six transition/transversion pathways.

222 ydrocarbon carcinogen benzo(a)pyrene display transversion point mutations in the DNA-binding domain o

223 had a G-->A transition and the other a G-->T transversion, possibly associated with error-prone misma

224 A strong contribution of C>A transversions, potentially due to oxidized bases, was al

225 AT>CG transversions predominated for the T-glycosylase.

226 paper sensor, we used it to identify a G > C transversion present in human genomic DNA from a ductal

227 Spontaneous G:C-->T:A transversions, previously not measured using reporter tr

228 s in all eight cases revealed an increase in transversions, probably due to DNA damage caused by cyto

229 rts only direct RNA substrates and the C-->G transversion provides an important criterion for target

230 Our DeltamutT allele elevates the AT-->CG transversion rate 27,000-fold, consistent with published

231 cleotide transition and an increased C --> A transversion rate.

232 hybrid progeny had decreased T-->G and T-->A transversion rates but an increased C-->T transition rat

233 We show that the transition and transversion rates in the 2 subgroups are similar, sugge

234 creasing number of plant studies revealing a transversion rather than transition bias, we chose to pe

235 d transitions over transversions (transition-transversion ratio = 1.29).

236 mutation spectrum, such as the transition to transversion ratio and AT mutational bias.

237 erate nucleotide sites and the transition-to-transversion ratio is described.

238 vs 1.41, P < .001), (2) higher transition to transversion ratio than would be expected if mutations w

239 rate and the mutational spectrum (transition/transversion ratio) of non-CpG residues change in parall

240 in the nucleotide composition and transition/transversion ratio.

241 e variant sets when comparing the transition/transversion ratios (p = 1.0), percentage of novel varia

242 ide screens of paralog groups and transition/transversion ratios highlighted genes including: green f

243 ty shift assays demonstrated that these same transversions reduced the affinity of the toxT promoter

244 show that MNMs exhibit a high percentage of transversions relative to transitions, findings that are

245 dAMP and dGMP (encoding G --> T and G --> C transversions, respectively).

246 r X family polymerases: a high proportion of transversions resulting from T.dTTP, T.dCTP, and C.dTTP

247 transversions and GC-->AT transitions, with transversions showing a strong strand bias and a remarka

248 B(1)-exposed cells that contained the G to T transversion signature mutation at their third base posi

249 itions occurred at roughly twice the rate of transversions, similar to results from sequence comparis

250 r the first time, we detected transition and transversion single nucleotide polymorphisms, as well as

251 uttle vector in COS-7 cells produces G --> T transversions slightly more frequently than does OxodG.

252 o correct coding sequences of 174 pathogenic transversion SNVs with >=90% precision.

253 T promoter derivatives with single-base-pair transversions spanning the TcpP-binding site were genera

254 , promoter derivatives with single-base-pair transversions spanning the ToxR-footprinted region were

255 om the breakpoint junctions, and favor C > G transversion substitutions; results suggest that single-

256 A single nucleotide transversion (T --> A) at the second position of intron

257 or mutations that were observed were G --> T transversions targeting the cross-linked dG located in t

258 alyses and showed a stronger relationship to transversion than transition mutations.

259 rsion bias, which is the preference for some transversions than others in nucleotide substitutions.

260 One transversion that abolishes secretion, uridyl 9 to adeny

261 report here that Dilp2 is caused by a T-to-A transversion that converts a tyrosine codon to a stop co

262 The single LF1 mutant allele is caused by a transversion that produces an amber stop at codon 87.

263 beta(2)m genes contained a single nucleotide transversion that would mutate a conserved alanine to pr

264 rized by predominant induction of G:C to T:A transversions that occurred within CpG sequence contexts

265 Homozygous mutant embryos carry a C->A transversion, that changes a threonine to a lysine, in a

266 ses in the relative frequency of G:C --> T:A transversions, the signature mutations of oxidative DNA

267 ifferent mechanisms generate transitions and transversions, these results indicate that both mutation

268 The transition/transversion (Ti/Tv) ratio and heterozygous/nonreference

269 the preponderance of transitions relative to transversions to the higher rate of mutation at CpG dinu

270 motifs = 25.6%) and favored transitions over transversions (transition-transversion ratio = 1.29).

271 ase that increases the mutation rate and the transversion/transition ratio compared to the signal seq

272 is there evidence of an increased mutational transversion/transition ratio or coordinated evolution.

273 as scanned for causative mutations and a C>A transversion was identified at c.10063 (human ref NM_000

274 Moreover, the ratio of transitions to transversions was markedly increased compared with norma

275 an unusually high rate of G to C and C to G transversions was observed at the third (silent) positio

276 Saturation of synonymous transversions was predicted to be minimal at 20 years an

277 ns produced by B(a)PDE i.e., "G-->T + C-->A" transversions, was significantly enhanced when the B(a)P

278 sitions generally occur more frequently than transversions, we find that the most frequent transversi

279 A:T-to-G:C transitions and G:C-to-T:A transversions were 3.8 and 2.0 times, respectively, more

280 ucleotide CpG and the neighboring effects on transversions were complex.

281 in a recA730 lexA(Def) mutL background most transversions were dependent upon pols IV and V.

282 In addition, G to T transversions were induced significantly, at frequencies

283 n the frequency of alkylation-induced C to A transversions were observed, consistent with a mutator t

284 > T transversions were the only mutations observed above bac

285 For the C-glycosylase, GC>CG transversions were the predominant mutations, followed b

286 s such as ErrASE preferentially corrects C/G transversions whereas T7 Endonuclease I preferentially c

287 However, the C-->A transversion, which causes a T94K mutation in the NST1 p

288 This results in the propagation of G to T transversions, which are commonly observed somatic mutat

289 ost frequently induced mutations were A to T transversions, which were 43.9% for (+)-syn- and 38.8% f

290 the treated pre-senescent cells was G:C->T:A transversion, whose frequency was intensified in the tre

291 3 mutation spectrum, dominated by A:T to T:A transversions with mutations at dA residues located almo

292 tations, i.e., T to C transitions and T to A transversions with significant site-specificities, i.e.,

293 the treated immortalized cells was A:T->C:G transversion, with a unique sequence-context specificity

294 Transition mutations were favored over transversions, with C-->T and G-->A replacements togethe

295 ed targeted mutations, predominantly G --> T transversions, with overall frequencies of approximately

296 can efficiently induce targeted C-to-G base transversions, with reduced levels of unwanted C-to-W (W

297 generated by both stereoisomers were G --> T transversions, with some G --> A transitions.

298 p deletions, UV induced both transitions and transversions, with the latter type more highly represen

299 P1 was heterozygous for a transversion within the TBXA2R gene predictive of a D304

300 y polymerase with regard to the induction of transversions within specific sequence contexts.