ライフサイエンスコーパス: mutation rate

1 (an order of magnitude higher than the point mutation rate).

2 itude above estimates of eukaryotic per base mutation rate.

3 epair gene mutS that accelerated the genomic mutation rate.

4 several orders of magnitude higher than the mutation rate.

5 hould not occur in lineages with an elevated mutation rate.

6 effect was observed with increased sequence mutation rate.

7 epair gene mutS that accelerated the genomic mutation rate.

8 ethal, but results in slow growth and a high mutation rate.

9 is only partly explained by heterogeneity in mutation rate.

10 ns than expected from the average background mutation rate.

11 e is two orders of magnitude higher than the mutation rate.

12 gly depend on the assumed mutagen-associated mutation rate.

13 y and repeatedly alternate with decreases in mutation rate.

14 sponse against a virus with an extraordinary mutation rate.

15 ltimate elimination of a genetic modifier of mutation rate.

16 acterized by an approximate 50% beta-catenin mutation rate.

17 ons contribute little to the human germ-line mutation rate.

18 t STRs by comparing observed versus expected mutation rates.

19 e major force driving the quick evolution of mutation rates.

20 nking mutations with disease and determining mutation rates.

21 showed that germline methylation influences mutation rates.

22 s ( approximately 30 kb) associated with low mutation rates.

23 aphy and variation in both recombination and mutation rates.

24 e difficult to maintain in genomes with high mutation rates.

25 sis-specific gene expression levels and TP53 mutation rates.

26 ivated mismatch repair dramatically increase mutation rates.

27 view that selection fine-tunes gene-specific mutation rates.

28 cancer types that often have extremely high mutation rates.

29 ates a subpopulation of cells with increased mutation rates.

30 were mutated significantly above background mutation rates.

31 ancer, and the stem-cell and transition-cell mutation rates.

32 e pathogen populations replicating with high mutation rates.

33 sive form of ovarian cancer with high ARID1A mutation rates.

34 riminating hosts are reached with reasonable mutation rates.

35 pairs, some of which may have relatively low mutation rates.

36 an be confounded by high and highly variable mutation rates across a cohort of samples.

37 hromatin remodeler, shows one of the highest mutation rates across many cancer types.

38 timing, explain up to 86% of the variance in mutation rates along cancer genomes.

39 ow mutation numbers, suggesting that the low mutation rate among IGHV5-51 PCs is dictated by the BCR

40 on characteristics known to influence local mutation rate and a series of enrichment filters in orde

41 o extract important key information, such as mutation rate and conserved single-nucleotide polymorphi

42 We find mutation rate and effective population size estimates to

43 Using the somatic mutation rate and eIF4B protein level, we identified thr

44 tify 76 gene-drug interactions based on both mutation rate and fitness and find that these parameters

45 there are racial differences in the somatic mutation rate and gene expression of ccRCC tumors from w

46 uggest that the inverse relationship between mutation rate and genome size is a result of the tradeof

47 um antiviral strategy that exploits the high mutation rate and low mutational tolerance of many RNA v

48 l and two asexual populations with increased mutation rate and observe maintenance of beneficial muta

49 entify a strong negative association between mutation rate and population density across 70 years of

50 ified an inverse plastic association between mutation rate and population density at 1 locus in 1 spe

51 between various evolutionary factors such as mutation rate and population size.

52 experimentally validated for sgRNA-mediated mutation rate and protein knockout efficiency.

53 was significantly higher than the background mutation rate and replicated our findings in public data

54 Notably, the inter-individual variation in mutation rate and spectra are low, suggesting tissue-spe

55 orders of magnitude higher than the germline mutation rate and that both mutation rates are significa

56 was heavily influenced by the site-specific mutation rate and the number of mutable alleles.

57 rement, in each patient, of both the in vivo mutation rate and the order and timing of mutations.

58 ng driver regions is challenged by a varying mutation rate and uncertainty of functional impact.

59 lution has been whether differences exist in mutation rate and/or mutation spectra among HIV types (i

60 evels, excessive oxidation of DNA, increased mutation rates and accumulation of DNA damage, which are

61 estimates, we identified determinants of STR mutation rates and built a model to predict rates for ST

62 roach uses mutagenic drugs to increase viral mutation rates and burden viral populations with mutatio

63 However, mutation rates and characteristics of de novo indels and

64 ting cell death at the expense of increasing mutation rates and contributing to the onset and progres

65 omes and Measures: The comparison of somatic mutation rates and differences in RNA expression in whit

66 tructural features probably causing elevated mutation rates and do not contain driver mutations.

67 Likewise, there was no detectable change in mutation rates and efficacy of selection.

68 er of this Red King effect, whereas relative mutation rates and generation times have little effect.

69 The high mutation rates and more compact genomes of RNA viruses h

70 cer mutation profiles revealed lower overall mutation rates and more frequent mutations in RHOB and c

71 ages showed good linear relationship between mutation rates and peak height.

72 generating a panel of variants with distinct mutation rates and recombination ability, we demonstrate

73 Racial differences in somatic mutation rates and RNA expression were examined.

74 e examined for racial differences in somatic mutation rates and RNA expression.

75 We investigated genome-wide mutation rates and spectra in multi-sibling families.

76 lts show that the populations with increased mutation rate, and capable of sexual recombination, outp

77 nucleotide polymorphic (SNP) sites in size, mutation rate, and mechanisms of maintenance in natural

78 With this ABC we infer recombination rate, mutation rate, and recombination tract length of Bacillu

79 ticular, NGS has yielded direct estimates of mutation rates, and an unbiased and calibrated molecular

80 identified that correlate with site-specific mutation rates, and novel mechanistic biophysical models

81 d argue that organelle DNA repair processes, mutation rates, and population genetic landscapes are al

82 rogeneity, identify rare cell types, measure mutation rates, and, ultimately, guide diagnosis and tre

83 tic nevi syndrome, and associated cancers on mutation rate; and evaluation of cases with anamnestic u

84 Sexual recombination and mutation rate are theorized to play different roles in a

85 Hence, it is clear that the germinal mutation rates are a function of both maternal and pater

86 Here we show that mutation rates are higher in heterozygotes and in proxim

87 However, their mutation rates are not correlated, indicating that the u

88 key parameters such as the intermediate cell mutation rates are not individually identifiable from th

89 However, mutation rates are not uniform across each eukaryotic ge

90 First, in vivo mutation rates are orders of magnitude lower than raw se

91 han the germline mutation rate and that both mutation rates are significantly higher in mice than in

92 While base-substitution mutation rates are similar to those in other multicellul

93 Mutation rates are used to calibrate molecular clocks an

94 ay experience similar selection pressures on mutation rate as bacterial pathogens, particularly durin

95 strate an unexpected flexibility in cellular mutation rates as a response to changes in selective pre

96 in weakly discriminating hosts, the required mutation rates, assuming a single locus, are untenably h

97 yotes and bacteria, with up to 23-fold lower mutation rates at higher population densities.

98 gression and stability, leading to increased mutation rates at highly transcribed loci.

99 ation of such Pol-alpha tracts and increased mutation rates at specific sites.

100 rtant confounding factor is the variation in mutation rates between lineages and over evolutionary hi

101 t dating evolutionary events requires not "a mutation rate" but a precise characterization of how mut

102 1 is already known to have an extremely fast mutation rate, but a new study shows it to be more than

103 Bacteria often respond with elevated mutation rates, but little evidence exists of stable euk

104 onymous changes in a reporter gene can lower mutation rate by >80%.

105 vation of the DnaE1 PHP domain increases the mutation rate by more than 3,000-fold.

106 Here, we directly estimated the spontaneous mutation rate by sequencing new Drosophila mutation accu

107 ility to remove genetic variants that change mutation rates by small amounts or in specific sequence

108 Taken together, our findings suggest that mutation rate can evolve through genetic changes that al

109 These results show that mutation rates can be drastically increased or decreased

110 Our results suggest that mutation rates can evolve markedly over short evolutiona

111 Genomic instability and high mutation rates cause cancer to acquire numerous mutation

112 ating mutations predispose to a higher local mutation rate, clusters of genes dominantly under purify

113 The critical mutation rate (CMR) determines the shift between surviva

114 accounted for other known factors affecting mutation rate, controlling for population density can re

115 providing a framework for understanding how mutation rates depend on sex, age, and cell division rat

116 A growing body of evidence supports mutation rate dependence on the local DNA sequence conte

117 ure, featuring a 2.88-fold increased somatic mutation rate, depletion of context-specific C>T substit

118 poliovirus adapts most rapidly at an optimal mutation rate determined by the trade-off between select

119 from outbreak cases, we estimated the virus mutation rate, determined that person-to-person transmis

120 between human populations.Estimates of human mutation rates differ substantially based on the approac

121 lied to analyze the genome-wide somatic gene mutation rate difference between lung adenocarcinoma (LU

122 results could also be relevant for resolving mutation-rate discrepancies in human and to explain kata

123 Functional regions exhibit higher mutation rates due to CpG dinucleotides and show signatu

124 hether treatments that alter lifespan change mutation rates early during lifespan could provide suppo

125 Overall effect size of radiation on mutation rates estimated as Pearson's product-moment cor

126 Translating mutation rates estimated from pedigrees into substitutio

127 published literature, comprising hundreds of mutation rates estimated using phenotypic markers of mut

128 r population density can reduce variation in mutation-rate estimates by 93%.

129 ic validations, we harnessed MUTEA to derive mutation-rate estimates for 702 polymorphic STRs by trac

130 d no significant effects of selection on our mutation-rate estimates.

131 nes that have a non-synonymous to synonymous mutation rate even greater than immune-related genes.

132 A potentially revealing hypothesis for mutation-rate evolution is that natural selection primar

133 nge from increasing genome size despite high mutation rates, faster replication, more efficient selec

134 The mutation rate for a copy of the CAN1 gene integrated ont

135 amilies suggests these CNVs have a very high mutation rate for a protein-coding locus, with a mutatio

136 Strikingly, any higher mutation rate for head-on genes can be explained by diff

137 tistic M was employed in estimating relative mutation rate for the NAHR-mediated CNVs in human popula

138 close to its known wild-type mutation rate; mutation rates for additional organisms were also found

139 Based on the mutation rates for Ebola virus given its natural sequenc

140 analysis also reveals fitness landscapes and mutation rates for which finite populations are found in

141 e we determined the genome-wide STR germline mutation rate from a deeply sequenced human pedigree.

142 mes these limitations by disentangling prior mutation rates from evaluation of the likelihood of the

143 eveloped MUTEA, an algorithm that infers STR mutation rates from population-scale data by using a hig

144 A high mutation rate fuels adaptation but also generates delete

145 o triggering SCV emergence by increasing the mutation rate, H2O2 also selected for the SCV phenotype,

146 The germline mutation rate has been extensively studied and has been

147 In cancer research, background models for mutation rates have been extensively calibrated in codin

148 Microsatellite mutation rate, however, depends on the length and nucleo

149 e been based on the estimation of background mutation rate, impact on protein function, or network in

150 h asthma were highly mutated (7.2%), somatic mutation rate in atopic dermatitis was less than half as

151 Additionally, CPGs showed a higher mutation rate in both inherited diseases and cancer, and

152 etic profiling of 293 BCCs found the highest mutation rate in cancer (65 mutations/Mb).

153 Ps, p190A exhibits a significantly increased mutation rate in cancer remains to be determined.

154 The characteristic elevated C>T mutation rate in CpG sites has been related to 5-methylc

155 cific diversity is in part owing to a higher mutation rate in domains of high recombination/diversity

156 nation of one signal, an increased TCC-->TTC mutation rate in Europeans, indicates a burst of mutatio

157 ssovers; and copy-number instability, with a mutation rate in excess of 1 per 100 transmissions in so

158 he number of hotspot motifs, and perhaps the mutation rate in general, is expected to decay over time

159 to leukemic transformation by increasing the mutation rate in hematopoietic stem/progenitor cells (HS

160 se, we find an approximately 3.5-fold higher mutation rate in heterozygotes than in homozygotes, with

161 tion history and refuelled the debate on the mutation rate in humans.

162 es, but much less is known about the somatic mutation rate in multicellular organisms, which remains

163 nt with this, there being a ten times higher mutation rate in pathogen resistance genes, expected to

164 stematic profiling of the somatic background mutation rate in protein-coding mononucleotide microsate

165 e per generation with a significantly higher mutation rate in repetitive DNA.

166 To take into account of higher mutation rate in the microsatellite region compared to t

167 a mechanistic explanation for the increased mutation rate in the POLD1-R689W-expressing cells.

168 e present a pedigree-based estimation of the mutation rate in this species.

169 e the variation with tissue stiffness of the mutation rate in tumors.

170 utations but also efficiently quantifies the mutation rate in vivo.

171 viral load (P < 0.001) and a trend of higher mutation rates in "a" determinant of HBsAg than age-comp

172 cancer-associated SAMHD1 mutations increase mutation rates in cancer cells.

173 nuclear genome, and most strongly increases mutation rates in coding and late replicating sequences.

174 genes, this is correlated with increases in mutation rates in coding sequences and regulatory region

175 Both exhibit different mutation rates in different tissues.

176 e results are not consistent with changes in mutation rates in general mediating the influence of alt

177 nomics enables direct measurement of somatic mutation rates in human brain and promises to answer thi

178 cilia genes were found selectively with high mutation rates in LUSC, possibly implying the importance

179 Here, we present data on somatic mutation rates in mice and humans, obtained by sequencin

180 High levels of transcription stimulate mutation rates in microorganisms, and this occurs primar

181 effects of sex-specific generation times and mutation rates in species with two sexes.

182 this relationship causes ultrahigh localized mutation rates in specific homopolymeric stretch regions

183 at parental reproductive age affects somatic mutation rates in the progeny and, thus, that some form

184 al reproductive age has an effect on somatic mutation rates in the progeny, because these are rare an

185 ke the first direct comparison with germline mutation rates in these two species.

186 stems evolving under strong linkage and high mutation rates, including viruses and cancer cells.

187 This defect results in a moderate mutation rate increase in typical genes, and a larger in

188 The mutation rate increased synergistically when the POLD1-R

189 We found that the mutation rate increased synergistically when the R696W m

190 The mutation rate increased with paternal age in all familie

191 rum shifted toward oxidative damage, and the mutation rate increased.

192 Spontaneous base substitution mutation rates increased sevenfold upon the disruption o

193 of the viruses after high-MOI passages, and mutation rates increased under low-MOI-passage condition

194 the high mutational load experienced at high mutation rates inhibits genome growth, forcing the genom

195 We show that at low point mutation rate, insertions are significantly more benefic

196 r, in large populations with high beneficial mutation rates interference among different escape strai

197 translate pedigree-based estimates of human mutation rates into split times among extant hominoids (

198 four parents and 12 offspring, the estimated mutation rate is 2.0 x 10(-9) per base per generation.

199 ests have suggested that the influenza virus mutation rate is 2.7 x 10(-6) - 3.0 x 10(-5) substitutio

200 The rapid viral mutation rate is a key factor, but recombination may als

201 Mutation rate is about twice as large as the migration r

202 The results indicate that the somatic mutation rate is almost two orders of magnitude higher t

203 r all genomic regions the same pre-specified mutation rate is assumed, which has a significant impact

204 The maize spontaneous mutation rate is estimated to be 2.17 x 10(-8) 3.87 x 1

205 During cell division, the spontaneous mutation rate is expressed as the probability of mutatio

206 agreement with empirical data, we find that mutation rate is inversely correlated with genome size i

207 This effect of temperature on the mutation rate is not limited to Arabidopsis, as we obser

208 A higher deleterious mutation rate is observed in the pericentromeric regions

209 mescale of wolves and dogs and find that the mutation rate is substantially slower than assumed by mo

210 The mutation rate is therefore strictly regulated and often

211 The mutation rate is uniformly low in all of the tumours (me

212 Finally, we provide a genome-wide mutation rate map for medical and population genetics ap

213 ls no significant differences in the overall mutation rate, mutation signatures, specific recurrent p

214 00), the CMR is close to its known wild-type mutation rate; mutation rates for additional organisms w

215 s study therefore provides insights into the mutation rates, mutational processes and developmental o

216 P1 were observed in 21% of cases, with lower mutation rates observed in sarcomatoid MPM (P < 0.001).

217 five postzygotic cleavages and calculated a mutation rate of 1.3 mutations per division per cell.

218 r 550 generations, the strain exhibited the mutation rate of >/=1.3 x 10(-8) single nucleotide subst

219 ith high parental relatedness, we estimate a mutation rate of 1.45 +/- 0.05 x 10(-8) per base pair pe

220 We measured an overall mutation rate of 1.8 x 10(-4) s/n/r for PR8 (H1N1) and 2

221 The mutation rate of 13 subjects having no signs but positiv

222 We estimate a mutation rate of approximately 1.5 x 10(-8) SNVs per sit

223 tical model for the somatic background indel mutation rate of microsatellites to assess mutation sign

224 ificantly affect the transmissibility or the mutation rate of Mtb within patients and was not associa

225 rs, and novel strategies exploiting the high mutation rate of noroviruses.

226 f an organism could selectively increase the mutation rate of specific genes that are actively under

227 eutic keratectomy (PTK), also calculated the mutation rate of subjects with normal corneas, but posit

228 rate pedigree data, we estimated the de novo mutation rate of the horse MSY and showed that various m

229 It is mostly due to the high mutation rate of the mtDNA and limited repair mechanisms

230 tood, although it is thought to increase the mutation rate of the viral polymerase during replication

231 tion rate for a protein-coding locus, with a mutation rate of up to 5% per gamete.

232 om the same male lineage because of the high mutation rate of Y-STRs.

233 dent and orientation-specific differences in mutation rates of genes require the B. subtilis Y-family

234 Previous studies have estimated the mutation rates of highly polymorphic STRs by using capil

235 to estimate P -values while controlling the mutation rates of individual patients and genes similar

236 ational dynamics of highly mutable STRs, the mutation rates of most others remain unknown.

237 regeneration/transformation procedures, the mutation rates of regenerants and transformants were rel

238 Platinum-based chemotherapy elevated the mutation rates of SCCHN compared to chemotherapy-naive S

239 whole-genome sequencing data to estimate the mutation rates of Y chromosome STRs (Y-STRs) with 2-6 bp

240 ates of humans and great apes based on lower mutation rates of ~0.5 x 10(-9) per site per year.

241 erimental results highlight the influence of mutation rate on the genetic basis of phenotypic evoluti

242 ential effects of unexplained variability in mutation rates on false-positive driver gene predictions

243 ulk-genotyped biopsies may therefore suggest mutation rate or selection intensity variation even when

244 wing to species differences, for example, in mutation rates or historical biogeography.

245 oxidative DNA damage significantly impacted mutation rates or spectra.

246 Our estimate for the mutation rate per base pair per generation is 1.05 x 10(

247 Our data suggest that the mutation rate per cell division is higher during both ea

248 the effective population size and mu is the mutation rate per site per generation), which explains s

249 ning that there is indeed density-associated mutation-rate plasticity (DAMP) at multiple loci in both

250 mutagenesis or repair are required for this mutation-rate plasticity.

251 frican populations, suggesting that the high mutation rates play dominant roles in producing the low

252 nding on the time between samples: estimated mutation rates, plus diversity noted within patients acr

253 nants of evolutionary rate: generation time, mutation rate, population size, and the intensity of nat

254 This is at the lower end of exome mutation rates previously estimated in parent-offspring

255 Higher mutation rates promote early germline sequestration.

256 s is consistent with comparative measures of mutation rates, provides a simple explanation for the ex

257 by differentiated cells, which have a higher mutation rate-quantification of stem cell DNA damage and

258 monly heterozygous), might have low and high mutation rates, respectively.

259 RNA viruses typically have high mutation rates, resulting in frequent production of prot

260 Specifically, population mutation rates rise when cells experience higher stress

261 Because of their high mutation rates, RNA viruses and retroviruses replicate c

262 requencies observed here with reported viral mutation rates suggests a complex interplay of nucleotid

263 reliable, identifying most off-targets with mutation rates superior to 0.1 %, while the number of fa

264 binding residues had a significantly higher mutation rate than other parts of the protein.

265 enotypic markers give a more precise view of mutation rate than previously believed: having accounted

266 d to be low-fidelity enzymes, providing high mutation rates that allow for the rapid adaptation of RN

267 DT pathway in human cells leads to increased mutation rates that may contribute to the onset of cance

268 The estimated mutation rate - the lowest among vertebrates analyzed to

269 However, given the high viral mutation rate, the appearance of novel drug-resistant vi

270 However, since RNA viruses are prone to high mutation rates, the possibility that these viruses will

271 st an expected background of low genome-wide mutation rates, these results demonstrate a previously u

272 ameters, for instance, the scaled population mutation rate Theta=4N e mu for diploids or Theta=2N e m

273 e loss is often associated with an increased mutation rate, thus quickly erasing evidence from the ge

274 theory developed to explain the evolution of mutation rates to address this question and explore its

275 resulting in the largest collection of Y-STR mutation rates to date.

276 ons, and using our precise context-dependent mutation rates to predict long-term evolutionary pattern

277 aluation of the clinical implications of HPV mutation rates, transmission, clearance, and persistence

278 umulate in the population coincides with the mutation rate, u, at which they arise in individuals: K

279 By calibrating the mutation rate using our oldest dog, we narrow the timing

280 and robustness to the confounding effects of mutation rate variation and background selection.

281 e-specific mutational signatures, long-range mutation rate variation, and position-specific impact me

282 rce of all genetic variation, clarifying why mutation rates vary is crucial for understanding all are

283 Mutation rates vary within genomes, but the causes of th

284 The between-patient mutation rate was 0.26 SNPs/year (95% CI 0.21-0.31).

285 The mutation rate was 67 of 1032 patients (6.5%).

286 he combined effect of the drug and mutant on mutation rate was greater than predicted.

287 The mutation rate was higher in GIST alone than in synchrono

288 The observed mutation rate was in agreement with rates previously det

289 r genes by testing whether the nonsynonymous mutation rate was significantly higher than the backgrou

290 e ovarian cancer has a high frequency of p53 mutation rates, we decided to investigate the relationsh

291 justs for sample- and genomic locus-specific mutation rates, we identify recurrently mutated sites ac

292 Mutation rates were unable to be determined because the

293 The viral mutation rates were variable between patients but did no

294 gen with limited genetic diversity and a low mutation rate which lacks any evidence for HGT.

295 mic regions with higher H3K36me3 had a lower mutation rate, which was increased with SETD2 mutation.

296 stion by revealing unexpectedly low germline mutation rates, which imply that substitutions accrue mo

297 ted memory IgA B cells of blood showed lower mutation rates with biased usage of IGHV3-48 and IGHV5-5

298 (mutation accumulation experiments) and low mutation rates with strong selection (natural isolates).

299 using genomes evolved under regimes of high mutation rates with weak selection (mutation accumulatio

300 cancer, or on the assumed mutagen-associated mutation rate, within the generally-accepted ranges test