ライフサイエンスコーパス: mtDNA

1 mtDNA concentrations are increased in IPF BAL and plasma

2 mtDNA damage was measured by using quantitative PCR and

3 mtDNA provides a model population biomarker associated w

4 mtDNA restoration reversed this miRNA to parental level,

5 mtDNA was recognized by cyclic-GMP-AMP synthase (cGAS) i

6 mtDNA was structured by elevation only in Z. capensis.

7 We detected 20 mtDNA haplotypes from six Brazilian states, eight of whi

8 t whether cells lacking TOP1MT have aberrant mtDNA transcription, we performed mitochondrial transcri

9 dant-induced AEC OGG1(K338/341) acetylation, mtDNA damage, and apoptosis, whereas SIRT3 silencing pro

10 Inherited and acquired mtDNA mutations have recently been associated with autis

11 consequence, any researcher desiring to add mtDNA variant analysis to their investigations is forced

12 SG-ADVISER mtDNA is a fast and functional tool that allows for vari

13 We have developed SG-ADVISER mtDNA, a web server to facilitate the analysis and inter

14 s in fibrotic lungs and thereby augments AEC mtDNA damage and apoptosis.

15 tos- or bleomycin-induced lung fibrosis, AEC mtDNA damage, and apoptosis in wild-type mice were ampli

16 l role for SIRT3 deficiency in mediating AEC mtDNA damage, apoptosis, and lung fibrosis.

17 of the 10 patients with mutations affecting mtDNA-encoded structural subunits showed loss of NDUFB8,

18 Our results suggest that Parkin affects mtDNA levels in a mitophagy-independent manner.SIGNIFICA

19 Moreover, protein-altering mtDNA variants that are initially present at low frequen

20 mitochondrial lineages encompassing ancient mtDNA functional polymorphisms, termed haplogroups, have

21 ochondrial fragmentation and reduced ATP and mtDNA copy number in FECD.

22 t to two copies of nuclear chromosomes), and mtDNA deletions may be present on only a very small perc

23 as increased differentiation, cell death and mtDNA damage.

24 ion between variants at 39 mitonuc genes and mtDNA introgression frequency.

25 We used morphology and mtDNA to test for genetic differentiation between high-

26 previous studies, depending upon nuclear and mtDNA haplotype, the magnitude and direction of changes

27 Mitochondrial DNA (mtDNA) copy number and mtDNA deletions were increased significantly in PD patie

28 the presence of both sera from patients and mtDNA, reproduced a refractory state after endotoxin cha

29 sed mitochondrial superoxide production, and mtDNA depletion as well as aberrations of mitochondrial

30 shows that mitochondrial chaperone TRAP1 and mtDNA replicating protein SSBP1 were significantly down-

31 Using Wolbachia and mtDNA titre as a phenotype, I perform the first associat

32 I estimate Wolbachia and mtDNA titre in each genotype, and I find considerable va

33 elative to expectation in both Wolbachia and mtDNA, but only mtDNA shows evidence of a recent selecti

34 , and the relationship between Wolbachia and mtDNA, using a large inbred panel of Drosophila simulans

35 spite low genetic diversity in Wolbachia and mtDNA.

36 eatest number of introns observed in annelid mtDNA genomes, and possibly in bilaterians.

37 y cell type, although there is little if any mtDNA replication after fertilization until the embryo i

38 ryotic cell, contain their own DNA, known as mtDNA, which is inherited exclusively from the mother.

39 s in the composition of autosomal as well as mtDNA, X chromosome, and Y chromosome ancestries.

40 to a knock-in (KI) mouse model of authentic mtDNA disease, specifically, progressive mtDNA depletion

41 We aimed to define an association between mtDNA and fibroblast responses in IPF.

42 Furthermore, interplay between mtDNA and nuclear DNA has been found in cancer cells, ne

43 DNA expression and DNA methylation driven by mtDNA.

44 the synthesis of OXPHOS subunits encoded by mtDNA.

45 In contrast, 7S DNA, produced by mtDNA replication, was reduced in the Top1mt KO cells.

46 the mitochondrial electron transport chain, mtDNA-depleted cells still maintain mitochondria and man

47 nome, ignoring the mitochondrial chromosome (mtDNA).

48 those who were not, according to circulating mtDNA levels.

49 DNA with either FVB/NJ, C57BL/6J, or BALB/cJ mtDNA.

50 28S and 18S rRNA, Histone H3 protein and COI mtDNA.

51 the Saka and the Pazyryks, reveals a common mtDNA package comprised of haplogroups H/H5, U5a, A, D/D

52 Our data suggests that no common mtDNA mutation identifies metastatic cells; rather the m

53 Here we report the complete mtDNA of an archaic femur from the Hohlenstein-Stadel (H

54 EVs in the peripheral circulation containing mtDNA.

55 ntly more PPN cholinergic neurons containing mtDNA deletion levels exceeding 60%, a level associated

56 formaticians aiming to acquire (or contrast) mtDNA annotations via MToolBox.

57 nuclease-mediated gene mutation correction, mtDNA damage was no longer detectable.

58 mitochondrial-targeted bKu does not decrease mtDNA content in human MCF7 cells.

59 Multiple OXPHOS defects and decreased mtDNA copy number (40%) were detected in muscle homogena

60 s of human AML, treatment with ddC decreased mtDNA, electron transport chain proteins, and induced tu

61 If only a few mitochondria with defective mtDNA are left in the embryo and undergo extensive repli

62 We demonstrated mtDNA detection over seven consecutive days, achieving a

63 lically dormant populations with CAF-derived mtDNA(hi) EVs promoted an escape from metabolic quiescen

64 Previously we described mtDNA copy number depletion across many solid tumor type

65 present a method, termed MitoDel, to detect mtDNA deletions from NGS data.

66 Detecting mtDNA deletions requires special care.

67 strains having identical nDNA, but different mtDNA.

68 we hypothesized that there are differential mtDNA-driven changes in nuclear (n)DNA expression and DN

69 HST carries the deepest divergent mtDNA lineage that splits from other Neanderthals approx

70 ne, a Rho(0) line lacking mitochondrial DNA (mtDNA) and a Rho(0) line with restored mtDNA.

71 Mitochondrial DNA (mtDNA) biosynthesis requires replication factors and ade

72 Mitochondrial DNA (mtDNA) copy number and mtDNA deletions were increased si

73 commodity trade data and mitochondrial DNA (mtDNA) cytochrome oxidase I (COI) and cytochrome b (Cyt

74 n carriers have increased mitochondrial DNA (mtDNA) damage and after zinc finger nuclease-mediated ge

75 KO) had higher endogenous mitochondrial DNA (mtDNA) damage.

76 cumulation of large-scale mitochondrial DNA (mtDNA) deletions and chronic, subclinical inflammation a

77 y, we showed that partial mitochondrial DNA (mtDNA) depletion in different cell types induced mitocho

78 of animals, in which the mitochondrial DNA (mtDNA) from one strain has been introgressed into the nu

79 y quantify human-specific mitochondrial DNA (mtDNA) from raw untreated wastewater samples.

80 gap, we analyzed ancient mitochondrial DNA (mtDNA) from Scythians of the North Pontic Region (NPR) a

81 Mitochondrial DNA (mtDNA) genes are long known to be cotranscribed in polyc

82 In recent years mitochondrial DNA (mtDNA) has transitioned to greater prominence across div

83 pable of associating with mitochondrial DNA (mtDNA) in Arabidopsis thaliana Gain- and loss-of-functio

84 The levels of circulating mitochondrial DNA (mtDNA) in patients with AIS correlated with impaired inf

85 s (ROS), membrane damage, mitochondrial DNA (mtDNA) integrity, morphology, phenotype and cytokine sec

86 ds gradient of increasing mitochondrial DNA (mtDNA) introgression from the arctic/boreal L. timidus,

87 Mitochondrial DNA (mtDNA) is actively eliminated from the developing sperm

88 Mitochondrial DNA (mtDNA) is essential for cell viability because it encode

89 Mitochondrial DNA (mtDNA) is typically inherited from only one parent [1-3]

90 pathway, is essential for mitochondrial DNA (mtDNA) maintenance.

91 By causing mitochondrial DNA (mtDNA) mutations and oxidation of mitochondrial proteins

92 Human mitochondrial DNA (mtDNA) polymerase gamma (Pol gamma) is the only polymera

93 tification based on three mitochondrial DNA (mtDNA) regions amplified on DNA extracted from dairy pro

94 The mechanism of mitochondrial DNA (mtDNA) replication in Saccharomyces cerevisiae is contro

95 was tested using a major mitochondrial DNA (mtDNA) survey and sequencing of two nuclear markers (AME

96 ls through the release of mitochondrial DNA (mtDNA) to drive the production of cGAMP by cGAS.

97 finity of the Neanderthal mitochondrial DNA (mtDNA) to modern humans than Denisovans has recently bee

98 indicates that mammalian mitochondrial DNA (mtDNA) tolerates such replication errors.

99 nhanced glycolysis, while mitochondrial DNA (mtDNA) transcripts were decreased, without detrimental e

100 mouse (males), where the mitochondrial DNA (mtDNA) undergoes double-strand breaks only in dopaminerg

101 nts with ASD, the role of mitochondrial DNA (mtDNA) variation has remained relatively unexplored.

102 Alterations in mitochondrial DNA (mtDNA) were once thought to be predominantly innocuous t

103 tion of HOS cells lacking mitochondrial DNA (mtDNA) with functional exogenous mitochondria and select

104 ry, such as extracellular mitochondrial DNA (mtDNA), have not been identified in IPF.

105 ographic studies based on mitochondrial DNA (mtDNA), which have been interpreted as supporting expans

106 The synthesis of all 13 mitochondrial DNA (mtDNA)-encoded protein subunits of the human oxidative p

107 clear-encoded subunits, 7 mitochondrial DNA (mtDNA)-encoded subunits or 14 known CI assembly factors.

108 the maternally inherited mitochondrial DNA (mtDNA).

109 include reads containing mitochondrial DNA (mtDNA).

110 e of methylation marks on mitochondrial DNA (mtDNA); but their contribution in cancer is unidentified

111 ing DNA topological tensions produced during mtDNA transcription, but it appears to be dispensable.

112 e show that knockdown of the nuclear-encoded mtDNA polymerase (Pol gamma-alpha), Tamas, produces a mo

113 pe was associated with the acquisition of EV mtDNA, especially in cancer stem-like cells, expression

114 All species except C. cinereum exhibited mtDNA haplotype variation consistent with recent populat

115 mpanied by the accumulation of extracellular mtDNA.

116 ndrial topoisomerase IB (TOP1MT) facilitates mtDNA replication by removing DNA topological tensions p

117 emographic histories: 1) the 'local' Finnish mtDNA haplotypes yielding small and dwindling size estim

118 ions is forced to explore the literature for mtDNA pipelines, evaluate them, and implement their own

119 s as a topological barrier and regulator for mtDNA transcription and D-loop formation.

120 ent or mitochondrial replacement therapy for mtDNA disease.

121 rkers appeared to be sorted between the four mtDNA groups, and species delimitation analyses supporte

122 Human mitochondria contain a genome (mtDNA) that encodes essential subunits of the oxidative

123 contain a 16,569-base-pair circular genome (mtDNA) encoding 37 genes required for oxidative phosphor

124 t on expression of the mitochondrial genome (mtDNA) and coordination with expression of the nuclear g

125 Although mitochondrial genomes (mtDNA) accumulate elevated levels of mutations in cancer

126 d xenograft models) laden with whole genomic mtDNA as a mediator of this phenotype.

127 ivergent HST branch is indicative of greater mtDNA diversity during the Middle Pleistocene than in la

128 Hence, mtDNA haplogroup variation is an important risk factor f

129 high-profile attempts to prevent hereditary mtDNA disease through mitochondrial replacement therapy

130 ls) is linked to the acquisition of the host mtDNA.

131 How mtDNA replication is terminated and the newly formed gen

132 These observations provide insights into how mtDNA could be altering epigenetic regulation and thereb

133 However, mtDNA landscapes of all metastatic cells are characteriz

134 Human mtDNA contains three promoters, suggesting a need for di

135 for variant calling and annotation of human mtDNA data coming from NGS experiments.

136 Surprisingly, accurate detection of human mtDNA transcription initiation sites (TISs) in the heavy

137 ing is in agreement with the fact that human mtDNA replication, typically, is not initiated by a DSB.

138 A loss syndromes with mutations of the human mtDNA polymerase [14-16].

139 t introduction of a male fertility-impairing mtDNA haplotype into replicated populations of Drosophil

140 in this review, we highlight alterations in mtDNA, with a specific focus on polymorphisms associated

141 , and CVD associated with a 1-SD decrease in mtDNA-CN were 1.29 (95% CI, 1.24-1.33), 1.11 (95% CI, 1.

142 a minority of cancer types exhibit a drop in mtDNA expression but an increase in nuDNA expression of

143 axons and was associated with an increase in mtDNA levels (mutant and wild type).

144 e, but it was associated with an increase in mtDNA levels (mutant and wild-type) without altering mit

145 Moreover, this increase in mtDNA-encoded ETC gene expression was associated with en

146 ta is a mitochondrial polymerase involved in mtDNA maintenance and is required for mitochondrial home

147 SB) is a homotetrameric protein, involved in mtDNA replication and maintenance.

148 Mutations in mtDNA cause a range of pathologies, commonly affecting e

149 Mutations in mtDNA lead to muscular and neurological diseases and are

150 which displays a marked increase in rGMPs in mtDNA.

151 replicates mtDNA, plays a surprising role in mtDNA elimination.

152 Despite regional shifts in mtDNA haplogroups, we conclude from individuals sampled

153 An overall similarity in mtDNA lineages of the NPR Scythians was found with the l

154 toid cell lines (LCL) demonstrated increased mtDNA damage relative to age-matched controls.

155 Expression of LRRK2 G2019S induced mtDNA damage in primary rat midbrain neurons, but not in

156 ort the hypothesis that LRRK2 G2019S-induced mtDNA damage is LRRK2 kinase activity dependent, uncover

157 bKu expression also induces mtDNA depletion that eventually results in the formation

158 rk presents a protein family that influences mtDNA architecture and homologous recombination in plant

159 evidence for a role of SWIB5 in influencing mtDNA architecture and homologous recombination at speci

160 ddC treatment inhibited mtDNA replication, oxidative phosphorylation, and induce

161 ation is initiated by a DSB and bKu inhibits mtDNA replication by binding to a DSB at ori5, preventin

162 builds on our own experience in interpreting mtDNA variants in the context of sudden death and rare d

163 gicus, and Mus musculus) showed a human-like mtDNA transcription pattern, the invertebrate pattern (D

164 Several studies have linked mtDNA mutations to metastasis of cancer cells but the na

165 cultural hitchhiking, likely explain the low mtDNA diversity.

166 F-orf and M-orf, respectively inside F and M mtDNAs, which are hypothesized to participate in sex det

167 onstrating their contribution in maintaining mtDNA.

168 Subsequently, attempts to manipulate mtDNA have been galvanized, although with few robust adv

169 species replacement likely promoted massive mtDNA introgression.

170 We measured mtDNA concentrations in bronchoalveolar lavage (BAL) fro

171 contribute to SCS A-beta deficiency-mediated mtDNA instability.

172 RK2 kinase function in LRRK2 G2019S-mediated mtDNA damage, using both genetic and pharmacological app

173 his deletion, we developed a single-molecule mtDNA combing method.

174 HTR cells had acquired host-derived (murine) mtDNA promoting estrogen receptor-independent oxidative

175 g (GRO-seq and PRO-seq) and analyzed nascent mtDNA-encoded RNA transcripts in diverse human cell line

176 , yet it remains impossible to study nascent mtDNA transcripts quantitatively in vivo using existing

177 We demonstrate that a complete Neanderthal mtDNA replacement is feasible over this time interval ev

178 .4 vs. 1.0 mm diameter) compared with FVB/NJ mtDNA.

179 alysis of nonhuman organisms enabled de novo mtDNA sequence assembly, as well as detection of previou

180 Mitochondrial DNA copy number (mtDNA-CN), which represents the number of mitochondria p

181 we tracked changes in per-cell abundances of mtDNA mutations from normal to tumor cells in the same p

182 epidermis to accelerate the accumulation of mtDNA deletions in this skin compartment.

183 Addition of mtDNA-CN to the 2013 American College of Cardiology/Amer

184 itative, reference sequence-free analysis of mtDNA transcription in all eukaryotes.

185 A phylogeny of Wolbachia and of mtDNA suggest a recent origin of the infection derived f

186 a), Tamas, produces a more complete block of mtDNA elimination.

187 a drop in respiratory activity: depletion of mtDNA copy number, decreases in mtRNA levels, and decrea

188 -scale deletions and a dramatic depletion of mtDNA in the epidermis and showed macroscopic signs of s

189 ular process have centered upon depletion of mtDNA through chemical or genetic means.

190 ecies show habitat-specific distributions of mtDNA haplotypes, probably the result of mother-offsprin

191 ial systems have remarkably low diversity of mtDNA.

192 sorder, which parallels previous evidence of mtDNA variation in other neurological diseases.

193 Expression of mtDNA entails multi-step maturation of precursor RNA.

194 ssing NT-PGC-1alpha had higher expression of mtDNA-encoded ETC genes than PGC-1alpha(-/-) brown adipo

195 iated replication is the predominant form of mtDNA replication in rho+ yeast cells.

196 acilitate the analysis and interpretation of mtDNA genomic data coming from next generation sequencin

197 here is little tendency for introgression of mtDNA to be harmful.

198 ellanicus, elevational movements and lack of mtDNA structure contrast with striking morphological div

199 polyploid, cells with advantageous levels of mtDNA mutations can be selected for depending on their c

200 asts, is associated with excessive levels of mtDNA.

201 Mutations within POLG impede maintenance of mtDNA and cause mitochondrial diseases.

202 However, the mechanism of mtDNA movement between cells remains unresolved.

203 rental inheritance (DUI) describes a mode of mtDNA transmission widespread in gonochoric freshwater m

204 24 cancer types to characterize patterns of mtDNA mutations and elucidate the selective constraints

205 ompassing the noncoding regulatory region of mtDNA in human and murine cells and tissues.

206 nge expansion, particularly in the region of mtDNA introgression.

207 process is suppressed by a key regulator of mtDNA-the transcription factor TEFM.

208 n origin are thought to drive replication of mtDNA by generation of an RNA primer.

209 tch between transcription and replication of mtDNA.

210 A putative role of mtDNA as a new biomarker of stroke-associated infections

211 considerations for investigating the role of mtDNA in cancer progression for future studies.

212 h underlying changes in epigenetic status of mtDNA that can subsequently results in induction of canc

213 of D-loop on the mtDNA and transcription of mtDNA-encoded genes.

214 The horizontal transfer of mtDNA and its role in mediating resistance to therapy an

215 demonstrated that the horizontal transfer of mtDNA from EVs acts as an oncogenic signal promoting an

216 To determine whether the transfer of mtDNA involves whole mitochondria, we injected B16rho(0)

217 s below) used to prevent the transmission of mtDNA-based disorders.

218 esent a crucial therapy for the treatment of mtDNA-driven, and some nuclear DNA-driven, mitochondrial

219 te for separation of the segregating unit of mtDNA, the nucleoid, within the mitochondrial network.

220 ggesting a direct effect of NT-PGC-1alpha on mtDNA transcription.

221 D1994A mutant (kinase dead) had no effect on mtDNA damage in either midbrain or cortical neuronal cul

222 Expression of genes encoded on mtDNA are altered in cancer cells, along with increased

223 tation in both Wolbachia and mtDNA, but only mtDNA shows evidence of a recent selective sweep or popu

224 incorporation is associated with early-onset mtDNA depletion in liver and late-onset multiple deletio

225 partial defects in either the nuclear DNA or mtDNA genes or combinations of the two can be sufficient

226 ion and degradation of HIF-1alpha in partial mtDNA-depleted cells.

227 te mtCOI and rRNA genes, and various partial mtDNA genes.

228 MRT aims to avoid pathogenic mtDNA transmission between generations by maternal spind

229 ed on limiting the inheritance of pathogenic mtDNA by mitochondrial replacement therapy (MRT).

230 y, preventing the transmission of pathogenic mtDNA mutations from mother to child is now a reality wi

231 U encompass 55% of the European population, mtDNA lineages must make a significant contribution to o

232 We have identified three potential mtDNA lineage ancestries of the NPR Scythians tracing ba

233 tion by binding to a DSB at ori5, preventing mtDNA segregation to daughter cells.

234 rsistently to mtDNA DSBs, thereby preventing mtDNA replication or repair.

235 nt ribonucleotide incorporation is a primary mtDNA abnormality that can result in pathology.

236 iate stalled mtDNA replication and can prime mtDNA replication from nonconventional origins.

237 with cancer susceptibility and/or prognosis, mtDNA as cancer biomarkers, and considerations for inves

238 tic mtDNA disease, specifically, progressive mtDNA depletion syndrome, resulting from a mutation in t

239 These mtROS damage mitochondrial proteins, mtDNA, and membrane lipids and release them in the cytos

240 lower boundary for the time of the putative mtDNA introgression event.

241 e orthogonal RNA-sequencing data to quantify mtDNA expression (mtRNA), and report analogously lower e

242 Our analyses suggest that rearranged mtDNAs appeared early during unionid radiation, and that

243 wn of cytoplasmic nucleoside kinases reduced mtDNA levels in AML cells, demonstrating their contribut

244 ne nucleoside kinase activity that regulates mtDNA biogenesis and can be leveraged to selectively tar

245 al DNA polymerase, which normally replicates mtDNA, plays a surprising role in mtDNA elimination.

246 The analysis of replicating mtDNA molecules provided in vivo evidence in support of

247 Del can detect novel and previously-reported mtDNA deletions.

248 urrent results differ from studies reporting mtDNA depletion in nigral dopaminergic neurons of PD pat

249 connection between metabolic reprogramming, mtDNA, fibroblast activation, and clinical outcomes that

250 life span of Tk2-deficient mice and restored mtDNA copy number as well as respiratory chain enzyme ac

251 bitor GNE-7915, either prevented or restored mtDNA damage to control levels.

252 DNA (mtDNA) and a Rho(0) line with restored mtDNA.

253 in TOP3A, characterized by muscle-restricted mtDNA deletions and chronic progressive external ophthal

254 Blocking or reversing mtDNA damage via LRRK2 kinase inhibition or other therap

255 A comparison of NPR Scythian mtDNA linages with other contemporaneous Scythian groups

256 We propose that the ability of selected mtDNA species to activate the UPR(mt) is a process that

257 task to assess the pathogenicity of specific mtDNA mutations.

258 in vitro that PrimPol can reinitiate stalled mtDNA replication and can prime mtDNA replication from n

259 tRNAs and precursor RNA encoded in L-strand mtDNA.

260 sed to detect four geographically structured mtDNA clusters.

261 Our data indicate that mtDNA replication termination occurs via a hemicatenane

262 Here, we show that mtDNA of solid tissues contains many more embedded ribon

263 ndrial Nuclear Exchange (MNX)-we showed that mtDNA could alter mammary tumor metastasis.

264 Recent evidence suggests that mtDNA undergo naturally occurring alterations, including

265 The mtDNA alterations led to an imbalanced stoichiometry of

266 The mtDNA depleted cells, with inhibited HIF-1alpha, showed

267 ar DNA from one inbred mouse strain, and the mtDNA from a different inbred mouse strain to examine th

268 moval of ribonucleotides incorporated by the mtDNA polymerase.

269 Illumina HumanHap 550 chip to determine the mtDNA haplogroups of the individuals.

270 Embedded rGMPs are expected to distort the mtDNA and impede its replication, and elevated rGMP inco

271 e, we do not observe a major turnover in the mtDNA record of the Iberian Late Chalcolithic and Early

272 found that miR-663 was down-regulated in the mtDNA-depleted Rho(0) line.

273 s Top3alpha as an essential component of the mtDNA replication machinery and as the first component o

274 machinery and as the first component of the mtDNA separation machinery.

275 stasis of cancer cells but the nature of the mtDNA species involved remains unclear.

276 fically enriched at the D-loop region of the mtDNA, which contains the promoters for several essentia

277 hanges in epigenetic status of D-loop on the mtDNA and transcription of mtDNA-encoded genes.

278 ing of the mitochondrial clades based on the mtDNA open reading frame (ORF).

279 uary 2017, we analyzed the data and used the mtDNA single-nucleotide polymorphisms interrogated by th

280 xchange data, we then determined whether the mtDNA haplogroups correlate with ASD risk.

281 While the mtDNA damage phenotype can be unambiguously attributed t

282 ution of DUI and of ORFans, we sequenced the mtDNAs of four unionids (two gonochoric with DUI, one go

283 ing mutations is largely determined by their mtDNA genomic landscapes, which can act either as an enh

284 lts show that intact mitochondria with their mtDNA payload are transferred in the developing tumour,

285 We demonstrate for all three mtDNA alignments that 3D projections significantly incre

286 Exposure to mtDNA augments alpha-smooth muscle actin expression in N

287 is found in large particles that localize to mtDNA during genome elimination.

288 pothesis that bKu would bind persistently to mtDNA DSBs, thereby preventing mtDNA replication or repa

289 is system, both female- and male-transmitted mtDNAs, named F and M respectively, coexist in the same

290 sis into L. timidus territory could underlie mtDNA introgression, and whether nuclear genes interacti

291 apamycin, while not targeting the underlying mtDNA defect, could represent a crucial therapy for the

292 , as well as detection of previously unknown mtDNA TIS, pausing, and transcription termination sites

293 samples and identified 55% with upregulated mtDNA biosynthesis pathway expression compared with norm

294 Using mtDNA quantification, enumeration of mitochondrial nucle

295 To determine whether mtDNA-CN, measured in an easily accessible tissue (buffy

296 need a better understanding of how and which mtDNA is tagged for replication versus transcription aft

297 on (NPR) and successfully retrieved 19 whole mtDNA genomes.

298 s predominantly in children as myopathy with mtDNA depletion.

299 lung fibroblasts (NHLFs) to stimulation with mtDNA and determined whether the glycolytic reprogrammin

300 This data supports the idea that yeast mtDNA replication is initiated by a DSB and bKu inhibits