ライフサイエンスコーパス: heteroplasmy

1 gation of the mutated and wild-type genomes (heteroplasmy).

2 ations coexist with wild-type genomes (mtDNA heteroplasmy).

3 tDNAs often co-exist in the same cell (mtDNA heteroplasmy).

4 tant and wild-type alleles within each cell (heteroplasmy).

5 ant and nonmutant mtDNA (a phenomenon called heteroplasmy).

6 e frequencies of mitochondrial genotypes and heteroplasmy.

7 t and wild-type mtDNAs coexist, resulting in heteroplasmy.

8 wild-type mtDNA, a situation known as mtDNA heteroplasmy.

9 sts with wild-type mtDNA, resulting in mtDNA heteroplasmy.

10 ally derived copies of the genome; a type of heteroplasmy.

11 eal the unexpectedly dynamic nature of human heteroplasmy.

12 well correlated with independent measures of heteroplasmy.

13 egion had nucleotide heteroplasmy and length heteroplasmy.

14 sequenced for nucleotide variants and length heteroplasmy.

15 ic and functional improvements in m.10191T>C heteroplasmy.

16 ations have largely been attributed to mtDNA heteroplasmy.

17 tain the wild-type mtDNA, a condition called heteroplasmy.

18 mutant mtDNA can co-exist in a state called heteroplasmy.

19 e mitochondrial genome, a condition known as heteroplasmy.

20 e accumulation of mtDNA length variation and heteroplasmy.

21 cantly higher levels of length variation and heteroplasmy.

22 7C, T146C, and T195C, at levels up to 70-80% heteroplasmy.

23 d subpopulation of mtDNA, a situation termed heteroplasmy.

24 tion of mitochondrial DNA mutations with low heteroplasmy.

25 donor and recipient cytoplasms, resulting in heteroplasmy.

26 anelle gene diversity and the maintenance of heteroplasmy.

27 ame cell-a phenomenon known as intracellular heteroplasmy.

28 ach pair, both members had similar levels of heteroplasmy.

29 etected, including one case of mitochondrial heteroplasmy.

30 aplogroup were associated with the extent of heteroplasmy.

31 ase could be sufficient to permanently alter heteroplasmy.

32 ry fibroblasts from patients with m.10191T>C heteroplasmy.

33 o the evolutionary dynamics of mitochondrial heteroplasmy.

34 to recognize and select against deleterious heteroplasmies.

35 e similar characteristics as found for human heteroplasmies.

36 id, directional, and complete shift in mtDNA heteroplasmy (2-6 h).

37 For deleterious heteroplasmies, a severe bottleneck may abruptly transfo

38 We observed a broad range of heteroplasmy across all cell types but also found marked

39 The difference in the frequency of heteroplasmy across different age groups was statistical

40 s the exploration, analysis and discovery of heteroplasmy across multiple genomic samples.

41 Cumulatively, mitochondrial heteroplasmy across the genome increased significantly w

42 mtDNA heteroplasmy also affects mitochondrial NAD(+)/NADH rati

43 ompound heterozygote and mtDNA homoplasmy or heteroplasmy), among whom 7,896 (4.375%) passed hearing

44 e cellular pathology at high levels of mtDNA heteroplasmy, an mtDNA deletion must accumulate to level

45 luation data shows that mtDNA-Server detects heteroplasmies and artificial recombinations down to the

46 e of droplet digital PCR (ddPCR) to validate heteroplasmies and confirm a de novo mutation.

47 191T>C cells had persistent improvements and heteroplasmy and a corresponding increase in maximal mit

48 ha-ketoglutarate levels increase at midlevel heteroplasmy and are inversely correlated with histone H

49 We simultaneously assayed single-cell heteroplasmy and cell state in thousands of blood cells

50 nd segregation that underlie cellular/tissue heteroplasmy and clinical variability.

51 We validated the underlying heteroplasmy and contamination detection model by genera

52 l impact to ongoing studies of mitochondrial heteroplasmy and disease.

53 s for an accurate detection of mitochondrial heteroplasmy and for the identification of variants asso

54 The noncoding MT-Dloop region had nucleotide heteroplasmy and length heteroplasmy.

55 This result, together with an absence of heteroplasmy and length variation in Gulf sturgeon mtDNA

56 es present in individual samples result from heteroplasmy and not from contamination.

57 results shed new light on the maintenance of heteroplasmy and provide a novel platform to investigate

58 standing of mitochondrial DNA control region heteroplasmy and provide additional empirical informatio

59 Heteroplasmy and recombination between divergent haploty

60 phisms have suggested a relationship between heteroplasmy and somatic aging.

61 Based on the presence of heteroplasmy and the recessive nature of these mutations

62 To broadly explore the variation of human heteroplasmy and to clarify the dynamics of somatic hete

63 lular proportion of mutated mtDNA molecules (heteroplasmy), and cell-to-cell variability in heteropla

64 f mutant and wild-type mtDNA (a state termed heteroplasmy), and the clinical features of the disease

65 s along with wild-type genomes in a state of heteroplasmy, and are a cause of severe inherited syndro

66 On average, each individual carried one heteroplasmy, and one in eight individuals carried a dis

67 Mitochondrial DNA (mtDNA) heteroplasmies are associated with various diseases but

68 These novel heteroplasmies are enhanced for tRNA and rRNA genes, and

69 Changing levels of mtDNA heteroplasmy are fundamentally related to the pathophysi

70 explained = 0.48%) suggesting site-specific heteroplasmy as a possible link between stress and incre

71 ay help understand the mechanisms generating heteroplasmy as well as its effects on plant phenotypes.

72 ence reads to identify sequence variants and heteroplasmy, as well as de novo sequence assembly.

73 tance that are suggestive of more widespread heteroplasmy at both atpA and cox1.

74 s sufficiently high that there is persistent heteroplasmy at nt 16192 in maternal lineages and at the

75 ols for analyzing, exploring and visualizing heteroplasmy at the genome-wide level in other taxonomic

76 ency of occurrence, and degree of associated heteroplasmy, but each includes the control region and o

77 tic mega-NUMTs can resemble paternally mtDNA heteroplasmy, but find no evidence of paternal transmiss

78 Using Mseek, we confirmed the ubiquity of heteroplasmy by analyzing mtDNA from a diverse set of ce

79 drial genome is possible, even low levels of heteroplasmy can affect the stability of the mtDNA genot

80 aining a tissue, that intermediate levels of heteroplasmy can be more detrimental than homoplasmy eve

81 This confirms that some mtDNA heteroplasmy can exist in human neurons, and provides th

82 lations show that the level of intracellular heteroplasmy can vary greatly over a short period of tim

83 here co-existing mutant and wild-type mtDNA (heteroplasmy) can be distinguished using restriction dig

84 The assay is not hindered by length heteroplasmy, can directly analyze template mixtures, an

85 ike episodes (MELAS) syndrome, the low mtDNA heteroplasmy causes maternally inherited diabetes with o

86 n MNRR1 levels compared to the wild type (0% heteroplasmy) (CL9), we evaluated the effects of MNRR1 l

87 This enables the inference of mtDNA heteroplasmy, clonal relationships, cell state and acces

88 al the dynamics of pathogenic mtDNA deletion heteroplasmy consistent with purifying selection and dis

89 Polyplasmy and heteroplasmy contribute to mitochondrial phenotypes and

90 s/cybrid cell, and the average percentage of heteroplasmy correlated well with the bulk cell sample.

91 Because heteroplasmy correlates with the severity and penetrance

92 We hypothesized that the stability of heteroplasmy could be facilitated by intercellular excha

93 P-seq data, the results of our mitochondrial heteroplasmy detection method suggest that mitochondrial

94 r workflow includes parallel read alignment, heteroplasmy detection, artefact or contamination identi

95 NA in ChIP-seq experiments is sufficient for heteroplasmy detection.

96 However, for some sites, observations of heteroplasmy did not mirror established mutation rate da

97 The frequency of heteroplasmy differed across tissue types, being higher

98 y, these data indicate that the frequency of heteroplasmy differs between particular populations, per

99 lustrate how MitoScape facilitates important heteroplasmy-disease association discoveries by expandin

100 non-synonymous substitutions, even at modest heteroplasmy, disrupts mitochondrial function and dramat

101 plasmy even for a dysfunctional mutant, that heteroplasmy distribution (not mean alone) is crucial fo

102 Previously, our understanding of the heteroplasmy distribution has been limited to just the m

103 on random genetic drift, for the full mtDNA heteroplasmy distribution.

104 Since cybrid cell lines with 73% m.3243A > G heteroplasmy (DW7) display a significant reduction in MN

105 mitophagy rate, and copy number to slow down heteroplasmy dynamics when mean heteroplasmy is low coul

106 ng near-complete directional shifts of mtDNA heteroplasmy, either by iterative treatment or through f

107 ers and homoplasmic fathers showed that once heteroplasmy enters a maternal lineage it is retained by

108 While the high mtDNA heteroplasmy exceeding a critical threshold causes mitoc

109 While several pipelines for analyzing heteroplasmies exist, issues in usability, accuracy of r

110 ources of mosaicism, including mitochondrial heteroplasmy, exogenous DNA sources such as vectors, and

111 oss individuals supports the hypothesis that heteroplasmy facilitates formation of novel mitochondria

112 It will further consider how this heteroplasmy facilitates recombination between genetical

113 ixation of heteroplasmic mtDNA, do levels of heteroplasmy fluctuate during life, is it possible to mo

114 We show incidences of heteroplasmy for mitochondrial atpA and patterns of inhe

115 ingly, we also observed the rapid changes of heteroplasmy frequencies during 4 weeks of the cell cult

116 However, the heteroplasmy frequencies from the same time point were h

117 childbirth, likely due to continued drift of heteroplasmy frequencies in oocytes under meiotic arrest

118 Meanwhile, the observed rapid-changing heteroplasmy frequency can potentially disturb cell func

119 We observed frequent drastic heteroplasmy frequency shifts between generations and es

120 in NO(2) was linked with MT-D-Loop(16311T>C) heteroplasmy from gestational weeks 17-25.

121 ith various diseases but the transmission of heteroplasmy from mtDNA to mitochondrial RNA (mtRNA) rem

122 nts, we developed a novel approach to detect heteroplasmy from the concomitant mitochondrial DNA frac

123 Dramatic tissue variation in mitochondrial heteroplasmy has been found to exist in patients with sp

124 Although heteroplasmy has been studied extensively in animal syst

125 The demonstration of universal mtDNA heteroplasmy has fundamental implications for our unders

126 development and maintenance of mitochondrial heteroplasmy has important consequences for both health

127 ioecious plant Plantago lanceolata, in which heteroplasmy has not previously been reported, and estim

128 Sharpley et al. show that heteroplasmy has surprising genetic and behavioral effec

129 teroplasmy), and cell-to-cell variability in heteroplasmy (heteroplasmy variance), remains incomplete

130 hondrial DNA (mtDNA) characteristics such as heteroplasmy (i.e. intra-individual sequence variation)

131 detection method suggest that mitochondrial heteroplasmies identified across vertebrates share simil

132 nto the architecture of the cfDNA, and mtDNA heteroplasmy identified in plasma provides new potential

133 a positive association between the number of heteroplasmies in a child and maternal age at fertilizat

134 ether with in vitro study indicates that the heteroplasmies in DNA can be transcribed into RNA with h

135 We compared heteroplasmies in mtRNA from 446 human B-lymphoblastoid

136 ncy (MAF) threshold of 2%, we identified 189 heteroplasmies in the trio mothers, of which 59% were tr

137 h 59% were transmitted to offspring, and 159 heteroplasmies in the trio offspring, of which 70% were

138 ce for rare chloroplast paternal leakage and heteroplasmy in 1.86% of the offspring.

139 Here, we study patterns of heteroplasmy in 2 tissues from each of 345 humans in 96

140 in 180 twin pairs and found evidence of site heteroplasmy in 4 pairs.

141 nvincingly documented cases of mitochondrial heteroplasmy in a small set of wild and cultivated plant

142 is highlighted by a progressive increase in heteroplasmy in a stem cell line derived from a PNT blas

143 al genes and within atp1, implying transient heteroplasmy in ancestral lineages.

144 Tissue levels of T8993C mutant heteroplasmy in blood and hair follicles were quantified

145 The degree of heteroplasmy in blood correlated well with the severity

146 thy at birth, with no or low levels of mtDNA heteroplasmy in blood.

147 tDNA deletions and investigating the role of heteroplasmy in cell-to-cell heterogeneity in cellular m

148 positions (nps) exhibit high frequencies of heteroplasmy in different tissues, and, moreover, hetero

149 different percentage levels of mutant mtDNA heteroplasmy in different tissues, but the factors influ

150 While the importance of mitochodrial heteroplasmy in human disease is unquestioned, we remain

151 Heteroplasmy in human mtDNA may play a role in cancer, o

152 ion was used to investigate the frequency of heteroplasmy in human mtDNA.

153 w reports the levels of inheritance of mtDNA heteroplasmy in humans and also explores mechanisms that

154 This study indicates that low-level heteroplasmy in HV1 is relatively common and that it occ

155 The single-cell analysis also revealed that heteroplasmy in individual cells is highly heterogeneous

156 Heteroplasmy in L2 was associated with a small variable

157 be an integrated cross-species evaluation of heteroplasmy in mammals that exploits previously reporte

158 on, which was present at very high levels of heteroplasmy in muscle (84%) and lower levels in blood (

159 We observed a significant shift in mtDNA heteroplasmy in muscle and brain transduced with recombi

160 a novel platform to investigate features of heteroplasmy in normal and diseased states.

161 pulations, to estimate the frequency of site heteroplasmy in normal human populations.

162 discussed with regard to previous studies of heteroplasmy in open-pollinated natural populations of S

163 We then detected mtDNA heteroplasmy in plasma from 3 patients.

164 s, and studied the dynamics of intracellular heteroplasmy in postmitotic cells.

165 Analysing 11,538 single cells shows stable heteroplasmy in sub-clones derived from the original don

166 l cell types but also found markedly reduced heteroplasmy in T cells, a finding consistent with purif

167 hose of other recent reports indicating that heteroplasmy in the control region is more common than w

168 A population study of heteroplasmy in the hypervariable region 1 (HV1) portion

169 Instances of point and length heteroplasmy in the mitochondrial DNA control region wer

170 Persistent heteroplasmy in the presence of antibiotics indicated th

171 We identify increased rates of heteroplasmy in women with MDD, and show from an experim

172 selection during transmission against novel heteroplasmies (in which the minor allele has never been

173 and the ratio of mutant to wild-type mtDNA (heteroplasmy) in each cell and tissue.

174 ogeneous, we found widespread heterogeneity (heteroplasmy) in the mtDNA of normal human cells.

175 drial DNA (mtDNA) often exists in a state of heteroplasmy, in which mutant mtDNA co-exists in cells w

176 Among children with ASD and PP heteroplasmies, increased mtDNA content shows benefits f

177 atistically significant, which suggests that heteroplasmy increases with age.

178 we show that, even though the low levels of heteroplasmy introduced into human oocytes by mitochondr

179 highly significant excess of liver-specific heteroplasmies involving nonsynonymous changes, most of

180 Heteroplasmy is a state in which more than one genome ty

181 We conclude that the observed heteroplasmy is an artifact.

182 The level of heteroplasmy is highly correlated with the number of yea

183 to slow down heteroplasmy dynamics when mean heteroplasmy is low could have therapeutic advantages fo

184 The role of mitochondrial heteroplasmy is of particular interest in plants as cyto

185 in the female germ line; despite this, mtDNA heteroplasmy is remarkably common.

186 colonies derived from single cells, we find heteroplasmy is stably maintained in individual daughter

187 oplasmy in different tissues, and, moreover, heteroplasmy is strongly dependent on the specific conse

188 Heteroplasmy is suspected to be common in flowering plan

189 Reducing heteroplasmy is therefore a therapeutic goal and in vivo

190 NA) coexisting within the same cell (a.k.a., heteroplasmy) is important in mitochondrial disease and

191 Mixing of mitochondrial DNAs (heteroplasmy) is unfavorable for reasons unknown.

192 rnally, and there are large random shifts in heteroplasmy level between mother and offspring.

193 ides into human mitochondria and thus impact heteroplasmy level in cells bearing a large deletion in

194 with the size of the deletion, the deletion heteroplasmy level in skeletal muscle, and the location

195 1), whereas no correlation was observed with heteroplasmy level or overall disease involvement.

196 amount of mutant mtDNA in a cell, called the heteroplasmy level, is an important factor in determinin

197 Understanding the distribution in heteroplasmy levels across a group of offspring is an im

198 Near-identical heteroplasmy levels in different tissues in both sibling

199 Resulting mice showed low heteroplasmy levels in multiple organs at adult age, nor

200 Heteroplasmy levels of the m.3243A>G mutation were measu

201 For example, increasing heteroplasmy levels of the mtDNA tRNA(Leu(UUR)) nucleoti

202 he mitochondrial DNA (mtDNA; m.3243A > G) at heteroplasmy levels of ~50 to 90%.

203 d deletions such as the "common deletion" at heteroplasmy levels well below 1%.

204 A comparison of age-corrected blood heteroplasmy levels with skeletal muscle, an embryologic

205 etabolic and epigenomic changes at different heteroplasmy levels, potentially explaining transcriptio

206 tecting large mitochondrial deletions at low heteroplasmy levels.

207 n the oocyte is the major determinant of the heteroplasmy MAF in the offspring.

208 ites than DZ twin pairs, suggesting that the heteroplasmy MAF in the oocyte is the major determinant

209 mtZFN-based approaches offer means for mtDNA heteroplasmy manipulation in basic research, and may pro

210 suggest that clinical manipulation of mtDNA heteroplasmy may be on the horizon for these largely unt

211 the potential mechanisms by which low mtDNA heteroplasmy may progressively cause diabetes mellitus.

212 Heteroplasmy might be achieved by one of two potential m

213 Since heteroplasmy might be difficult to detect should multipl

214 In certain circumstances heteroplasmy might be regulated at the level of the indi

215 se studies of Silene vulgaris suggested that heteroplasmy might occur in this species at a level that

216 At high heteroplasmy, mitochondrially derived acetyl-CoA levels

217 tistically significant higher levels of D310 heteroplasmy (more than one length variant) in the lymph

218 lysis revealed that the majority of detected heteroplasmies occur in intergenic regions.

219 Although heteroplasmy occurred at a total of 16 different positio

220 nfluences patterns of gene flow, and whether heteroplasmy occurs in natural populations at a frequenc

221 with mismatched primers was employed to show heteroplasmy of a novel 12SrRNA mutation in the proband

222 We reveal single-cell variation in heteroplasmy of a pathologic mtDNA variant, which we ass

223 aplotype sample, implying at least transient heteroplasmy of mitochondrial DNA (mtDNA).

224 , we generated mice containing an admixture (heteroplasmy) of NZB and 129S6 mtDNAs in the presence of

225 impact of mitochondrial paternal leakage and heteroplasmy on both the evolution of the mitochondrial

226 cterial genetics, such as genetic dominance, heteroplasmy or segregational drift.

227 Low-frequency mutations, heteroplasmies, or SNPs scattered throughout the DNA in

228 lasmy and to clarify the dynamics of somatic heteroplasmy over the course of lifespan, we analyzed mi

229 from human data to correct for the change in heteroplasmy over time.

230 For the other two patients, the heteroplasmy pattern is also different between plasma an

231 We identified 13,189 heteroplasmies (Phred score > 10,000, minor allele frequ

232 the percentage of normal and mutant mtDNAs (heteroplasmy) present within the cell.

233 We observed 2786 heteroplasmies presenting in both DNA and RNA at 1% freq

234 How quantitative differences in mtDNA heteroplasmy produces distinct pathological states has r

235 Heteroplasmy ranged from 15% to 63%.

236 pies of deleted mtDNA, and the percentage of heteroplasmy ranged from 43+/-16 to 95+/-16%.

237 Because of unique features such as heteroplasmy, replicative segregation, and threshold eff

238 , is responsible for the different levels of heteroplasmy seen in the offspring of heteroplasmic fema

239 Rapid shifts in the level of heteroplasmy seen within a single generation contribute

240 emove mutated mtDNA through the induction of heteroplasmy shift in oocytes and zygotes.

241 of mitochondrial diseases by inducing mtDNA heteroplasmy shift through the selective elimination of

242 at do not affect GQ formation did not induce heteroplasmy shift.

243 genomes in favor of the wild-type, known as heteroplasmy shifting, is potentially therapeutic.

244 l of these tissue-related and allele-related heteroplasmies show a significant age-related accumulati

245 two sequencing studies, and resequenced its heteroplasmy sites.

246 ative mitochondrial copy numbers and detects heteroplasmy, somatic mutation and structural variants o

247 random drift process underlying the shifting heteroplasmy, some reports describe differences in segre

248 ll, humans contain multiple mtDNA genotypes (heteroplasmy); specific patterns of variants accumulate

249 Similar treatment of pathogenic heteroplasmies that do not affect GQ formation did not i

250 nifestations vary based on mutation type and heteroplasmy (that is, the relative levels of mutant and

251 (mtDNA) diseases depends on the frequency of heteroplasmy (the presence of several alleles in an indi

252 It is increasingly appreciated that heteroplasmy, the occurrence of multiple mtDNA haplotype

253 Mitochondrial heteroplasmy, the presence of more than one mitochondria

254 Heteroplasmy, the presence of more than one type of mtDN

255 As a test for contamination and to confirm heteroplasmy, the samples were sequenced for the HVI reg

256 ith mitochondrial DNA (mtDNA) mutations, but heteroplasmy-the coexistence of mutant and wild-type mtD

257 Heteroplasmy-the presence of multiple mitochondrial DNA

258 In addition, in the presence of heteroplasmy there is a threshold whereby a certain leve

259 Significant regressions of heteroplasmy, theta and pi, on repeat number further sug

260 We tested the potential for shifting heteroplasmy through the cyclical application of two dif

261 ntal inheritance resulting in a low level of heteroplasmy) to 100% in others.

262 d repopulation and was effective in shifting heteroplasmy towards the non-pathogenic allele.

263 Here we present a high-resolution study of heteroplasmy transmission conducted on blood and buccal

264 Here, we analyze the dynamics of mtDNA heteroplasmy transmission in the Genomes of the Netherla

265 ing a mixture of mutant and wild-type mtDNA (heteroplasmy) transmit a varying proportion of mutant mt

266 We propose that in the context of mtDNA heteroplasmy, UPR(mt) activation caused by OXPHOS defect

267 onditions, the (genetic) rate of increase in heteroplasmy variance and de novo mutation are proportio

268 n experimental and computational research on heteroplasmy variance in different species.

269 Heteroplasmy variance is particularly important since it

270 nd cell-to-cell variability in heteroplasmy (heteroplasmy variance), remains incompletely understood.

271 , other diseases, and aging, but patterns of heteroplasmy variation across different tissues have not

272 t with earlier studies, but a higher rate of heteroplasmy varying between 10% and 50%.

273 The frequency of heteroplasmy was 5 of 43 individuals, or 11.6%.

274 Length heteroplasmy was also observed in the AC dinucleotide re

275 An initial search for heteroplasmy was conducted by use of the SSO probe syste

276 Point heteroplasmy was detected in approximately 6% of all sam

277 Evidence for heteroplasmy was found in 23 of the 99 individuals studi

278 As expected, length heteroplasmy was frequently observed in the HVI, HVII an

279 examining mother-child pairs, we found that heteroplasmy was inherited (30%) but could occur de novo

280 In general, the sites at which heteroplasmy was most commonly observed correlated with

281 Heteroplasmy was observed in 35 individuals (13.8%; 95%

282 Heteroplasmy was quantitated in individual cytoplasmic h

283 ed for five generations (F5), revealing that heteroplasmy was reduced in F2 mice and was undetectable

284 Accounting for heteroplasmies, we estimated the mtDNA germ-line mutatio

285 context and to explore general principles of heteroplasmy, we describe an integrated cross-species ev

286 To understand the nature of heteroplasmy, we developed Mseek, a novel technique to p

287 Among them, the frequencies of 2427 (87.1%) heteroplasmies were highly consistent (less than 5% freq

288 Significant levels of heteroplasmy were identified at 0.24% of sites evaluated

289 Surprisingly, changes in heteroplasmy were not uniform with some sites demonstrat

290 c proportions as low as 1% and virtually all heteroplasmy where the minor component is > or = 5%.

291 l detection method for accurate detection of heteroplasmies, which also accounts for the error rate o

292 l) ) gene, m.1661A>G, present at nearly 100% heteroplasmy, which disrupts a Watson-Crick base pair in

293 omic configurations that contribute to mtDNA heteroplasmy, which drives rapid evolution of the sequen

294 We identified 4,577 heteroplasmies (with an alternative allele frequency of

295 chondrial PstI caused a significant shift in heteroplasmy, with an accumulation of the mtDNA haplotyp

296 ght individuals carried a disease-associated heteroplasmy, with minor allele frequency >/=1%.

297 The evolution of heteroplasmy within a generation was studied in samples

298 fter mating, and temperature on evolution of heteroplasmy within and between generations.

299 ure of mutated and wild type genomes (termed heteroplasmy) within individual cells.

300 currently available, the ability to modulate heteroplasmy would have a major impact in the phenotype