ライフサイエンスコーパス: mtDNA

1 mtDNA can be profiled along with measures of cell state,

2 mtDNA depletion and cytochrome c oxidase-negative cells

3 mtDNA was recognized by the DNA sensor cGAS and generate

4 Here, using 4207 mtDNA sequences, we analysed the colonisation patterns a

5 mitochondrial DNA (mtDNA) although aberrant mtDNA rNMP content has been identified in disease models

6 Accordingly, mtDNA rNMPs were nearly absent in SAMHD1 (-/-) mice that

7 ious cancer clone that occasionally acquires mtDNA from its hosts.

8 sis due to unresolved RNA:DNA hybrids across mtDNA.

9 f rNMPs did not, however, appreciably affect mtDNA copy number or the levels of mtDNA molecules with

10 izes SSBP1 dimer/tetramer formation, affects mtDNA replication, and induces mtDNA depletion.

11 After mtDNA segregation, mtDNA transcription begins, which act

12 cal changes in recipient cells shortly after mtDNA transfer, but the long-term retention and function

13 d suggest little purifying selection against mtDNA deletions by mitophagy in postmitotic muscle fiber

14 e loss of mitochondrial activity and altered mtDNA copy number that result in organ dysfunction in ag

15 tween germline and somatic tissues and among mtDNA regions, suggestive of distinct mutagenesis mechan

16 Here, we show how an mtDNA sequence's balance between replication and transcr

17 pre-Roman individuals (obtaining 19 ancient mtDNAs) excavated from the necropolis of Plestia.

18 )O(2) production reduced in both depots, and mtDNA decreased in gSAT (p < 0.05).

19 Total DNA was isolated and mtDNA copy numbers were determined using absolute quanti

20 r mitochondrial copy numbers were lower, and mtDNA and Rac1 promoter DNA methylation was exacerbated.

21 served deletion patterns are best modeled as mtDNA deletions initiated by replication fork stalling d

22 NA, nucleoids, and 7S-DNA amounts as well as mtDNA replication, affecting replisome machinery.

23 We used DdCBEs to model a disease-associated mtDNA mutation in human cells, resulting in changes in r

24 methylation, which contributes to attenuated mtDNA transcription and a reduced mtDNA copy number.

25 Mitochondrial membrane protein p32 can block mtDNA synthesis by restricting RECQ4 mitochondrial local

26 DEC205 is a transmembrane protein that bound mtDNA and contributed to pattern recognition by Toll-lik

27 Remarkably, one canine mtDNA haplotype, A1d1a, has repeatedly and recently colo

28 rial DNA (mtDNA) replication machinery cause mtDNA depletion syndromes (MDSs), which associate ocular

29 entified MVs containing mitochondria and ccf-mtDNA was quantified by real-time PCR.

30 olation that considers both ccf-nDNA and ccf-mtDNA.

31 d a detailed protocol optimized for both ccf-mtDNA and ccf-nDNA recovery that uses a magnetic bead-ba

32 circulating cell-free mitochondrial DNA (ccf-mtDNA) in HIV-infected patients and controls.

33 irculating, cell-free mitochondrial DNA (ccf-mtDNA) is under similar investigation.

34 d efficiency of recovery of ~95-fold for ccf-mtDNA and 20-fold for ccf-nDNA when compared with the in

35 t high-throughput approach optimized for ccf-mtDNA and ccf-nDNA recovery and serves as an important s

36 ayed plate edge effects resulting in low ccf-mtDNA reproducibility, whereas ccf-nDNA was less affecte

37 However, optimal ccf-mtDNA isolation parameters have not been established, an

38 MV numbers correlated with ccf-mtDNA levels that were higher among HIV-infected patient

39 ortunity to poison proliferating cancer cell mtDNA replication as certain cancers rely heavily on mit

40 Cellular mtDNA content in PBMCs was higher than in peripheral blo

41 etes patients had similar levels of cellular mtDNA compared to healthy participants but a significant

42 hat the relationship between cellular and cf mtDNA content is affected by disease status.

43 direct relationship between cellular and cf mtDNA content within individuals.

44 f, and relationship between, cellular and cf mtDNA in human blood.

45 is important to measure both cellular and cf mtDNA.

46 y participants but a significantly higher cf mtDNA content.

47 al blood and a surprisingly high level of cf mtDNA was present in serum and plasma of HC, with no dir

48 f mitochondrial function, and cell-free (cf) mtDNA linked to inflammation.

49 t African (Acinonyx jubatus jubatus) cheetah mtDNA diverged approximately 72 kya, while the Southeast

50 t the most recent common ancestor of cheetah mtDNA is approximately twice as ancient as currently rec

51 hips by studying larger fragments of cheetah mtDNA, both from an Indian cheetah museum specimen and t

52 ican (Acinonyx jubatus soemmeringii) cheetah mtDNA diverged around 139 kya.

53 method for quantifying deletions in circular mtDNA molecules.

54 dative phosphorylation deficiency for common mtDNA variants and nuclear-encoded complex I variants an

55 on led to a reduced efficiency in completing mtDNA synthesis due to unresolved RNA:DNA hybrids across

56 ion can be explained by complex concatenated mtDNA-derived sequences rearranged within the nuclear ge

57 seq), a method that combines high-confidence mtDNA mutation calling in thousands of single cells with

58 xamine Twinkle disease variants and the core mtDNA replication machinery.

59 n event and occurs somatically on other CTVT mtDNA backgrounds.

60 Cytosolic mtDNA activated the cGAS/STING/IRF3 pathway, stimulating

61 Thus, we demonstrated that cytosolic mtDNA activated the inflammatory response in aging and n

62 In mice, decreased mtDNA levels were visualized in renal tubules as a funct

63 Ablation, the deleted mtDNA fraction, suffices to explain skeletal muscle phen

64 ession, we tested the role of cancer-derived mtDNA in a mechanism of paracrine signaling.

65 h in Saccharomyces cerevisiae, we determined mtDNA-to-nuclear DNA ratios in 5148 strains lacking none

66 How the transmission of detrimental mtDNA mutations is restricted through the maternal linea

67 This diachronic mtDNA portrait of Umbria fits well with the genome-wide

68 ion fork stalling during strand displacement mtDNA synthesis.

69 d analysis of nuclear and mitochondrial DNA (mtDNA) allows rapid diagnosis for the vast majority of p

70 of rNMPs is tolerated in mitochondrial DNA (mtDNA) although aberrant mtDNA rNMP content has been ide

71 lly acquired mutations in mitochondrial DNA (mtDNA) and consecutive respiratory chain dysfunction as

72 rradiation caused greater mitochondrial DNA (mtDNA) and nuclear DNA (nDNA) damage in female mice, ind

73 greater concentration of mitochondrial DNA (mtDNA) compared to noncancer epithelia.

74 e maintenance of multiple mitochondrial DNA (mtDNA) copies.

75 Mitochondrial DNA (mtDNA) copy number in leukocytes has been regarded as a

76 pedigree computation, and mitochondrial DNA (mtDNA) copy number inference.

77 cation and segregation of mitochondrial DNA (mtDNA) creates the potential for evolutionary conflict d

78 K2 G2019S mutation causes mitochondrial DNA (mtDNA) damage and is LRRK2 kinase activity-dependent.

79 drial toxicity, including mitochondrial DNA (mtDNA) depletion in several cases.

80 antation, associated with mitochondrial DNA (mtDNA) depletion without accumulation of multiple deleti

81 ncy, de novo mutations in mitochondrial DNA (mtDNA) directly from oocytes and from somatic tissues (b

82 Mitochondrial DNA (mtDNA) encodes cellular machinery vital for cell and org

83 Mitochondrial DNA (mtDNA) encodes proteins and RNAs that support the functi

84 d the association between mitochondrial DNA (mtDNA) haplogroups and the homeostatic model assessments

85 Although mitochondrial DNA (mtDNA) haplotype variation is often applied for estimati

86 ile analysis of 139 bp of mitochondrial DNA (mtDNA) has confirmed that the Indian cheetah was part of

87 The synthesis of mitochondrial DNA (mtDNA) is a complex process that involves the formation

88 we report that mammalian mitochondrial DNA (mtDNA) is enriched for 6mA.

89 Precise gene editing of mitochondrial DNA (mtDNA) is essential for the generation of model systems

90 tion the dogma that human mitochondrial DNA (mtDNA) is inherited exclusively down the maternal line,

91 Although mitochondrial DNA (mtDNA) is prone to accumulate mutations and lacks conven

92 ociated with one of three mitochondrial DNA (mtDNA) m.3460G>A, m.11778G>A and m.14484T>C mutations.

93 Somatic mitochondrial DNA (mtDNA) mutations accumulate with age in human tissues an

94 own about the spectrum of mitochondrial DNA (mtDNA) mutations across pediatric malignancies.

95 Furthermore, mitochondrial DNA (mtDNA) mutations associated with NADH dehydrogenase subu

96 Natural mitochondrial DNA (mtDNA) mutations enable the inference of clonal relation

97 Mutations of mitochondrial DNA (mtDNA) often underlie mitochondrial disease, one of the

98 Selfish or cheater mitochondrial DNA (mtDNA) proliferates within hosts while being selected ag

99 homeostasis, resulting in mitochondrial DNA (mtDNA) release and activation of cytosolic DNA-mediated

100 ondrial pores and induced mitochondrial DNA (mtDNA) release into the cytosol of endothelial cells.

101 f the molecular events in mitochondrial DNA (mtDNA) replication is crucial to understanding the origi

102 ncoding components of the mitochondrial DNA (mtDNA) replication machinery cause mtDNA depletion syndr

103 Mitochondrial DNA (mtDNA) resides in a high ROS environment and suffers mor

104 Alterations in mitochondrial DNA (mtDNA) sequence and copy number are implicated in aging

105 e genome sequencing, deep mitochondrial DNA (mtDNA) sequencing, and tested for mitochondrial deletion

106 chondrial dysfunction and mitochondrial DNA (mtDNA) variation in ME/CFS.

107 Here, we investigated the mitochondrial DNA (mtDNA) variation of 545 present-day Umbrians (with 198 e

108 -generation sequencing of mitochondrial DNA (mtDNA) was performed for 6 affected family members.

109 species (ROS) generation, mitochondrial DNA (mtDNA), and nuclear DNA (nDNA) damage).

110 Base editing within mitochondrial DNA (mtDNA), however, has thus far been hindered by challenge

111 the maternally inherited mitochondrial DNA (mtDNA), known to be highly informative for human ancestr

112 ich causes the release of mitochondrial DNA (mtDNA), thereby triggering inflammation.

113 Circulating mitochondrial DNA (mtDNA), widely studied as a disease biomarker, comprises

114 genetic variation within mitochondrial DNA (mtDNA).

115 replication and repair of mitochondrial DNA (mtDNA).

116 re caused by mutations in mitochondrial DNA (mtDNA).

117 roplasmic mutation in the mitochondrial DNA (mtDNA; m.3243A > G) at heteroplasmy levels of ~50 to 90%

118 is common in angiosperm mitochondrial DNAs (mtDNAs), few cases of functional foreign genes have been

119 approximately four 6mA modifications on each mtDNA molecule.

120 del(A420-A463) mutant, it failed to enhance mtDNA synthesis due to the accumulation of RNA:DNA hybri

121 conomical and generalized methods for entire mtDNA genome enrichment prior to high-throughput sequenc

122 Here, we evaluate mtDNA retention in new host cells using 'MitoPunch', a d

123 In conclusion, when evaluating mtDNA in human blood as a biomarker of mitochondrial dys

124 tribution of the H4a1 haplogroup in existing mtDNA, thus creating a baseline for future occurrences o

125 g uridine-free selection, although exogenous mtDNA is lost from metabolically impaired, mtDNA-intact

126 Uncovering factors that stabilize exogenous mtDNA integration will improve our understanding of in v

127 Our results suggest that exogenous mtDNA retention in metabolically impaired rho+ recipient

128 ne of older versus younger mice, arguing for mtDNA turnover during oocyte meiotic arrest.

129 1 during RGC differentiation is critical for mtDNA maintenance to produce appropriate optic nerve con

130 Q4 is a DNA replication factor important for mtDNA maintenance, and here, we unveil a role of human R

131 We found mtDNA mutation frequencies 2- to 3-fold higher in 10-mon

132 By contrast, circulating cell-free mtDNA concentrations in unaffected heterozygous carriers

133 -reactive protein, and circulating cell-free mtDNA in serum of 245 participants in two cohorts from t

134 r, the role of IL6 and circulating cell-free mtDNA in unaffected and affected individuals harbouring

135 levels; and (iv) that circulating cell-free mtDNA levels have good predictive potential to discrimin

136 in PRKN/PINK1, IL6 and circulating cell-free mtDNA levels may serve as markers of Parkinson's disease

137 tions; (iii) increased circulating cell-free mtDNA serum levels in both patients with biallelic or wi

138 lly to secure the transmission of functional mtDNA through Drosophila oogenesis.

139 xtent variation in the mitochondrial genome (mtDNA) contributes to the biological heterogeneity obser

140 Acquired human mitochondrial genome (mtDNA) deletions are symptoms and drivers of focal mitoc

141 e of HGT events in the mitochondrial genome (mtDNA).

142 iferating and differentiated HepaRG harbored mtDNA levels of 0.9% and 17.9% compared with control cel

143 The level of 6mA in HepG2 mtDNA is at least 1,300-fold higher than that in gDNA un

144 significant between groups with low and high mtDNA copy number (P < 0.001 and 0.002, respectively).

145 mtDNA copy number group (< median) and high mtDNA copy number group (>= median).

146 Acute depletion of Pim1 phenocopied the high mtDNA levels observed in Deltamrx6 cells.

147 ximal and distal tubules had markedly higher mtDNA levels compared with cells within glomeruli and co

148 itochondrial membrane potential, with higher mtDNA release in brain and primary cerebro-cortical neur

149 ids within the mitochondrial matrix, but how mtDNA nucleoids are formed and regulated within cells re

150 However, mtDNA replication is independent of the cell cycle creat

151 on segregation behaviour in mouse and human mtDNA.

152 hat catalyse C*G-to-T*A conversions in human mtDNA with high target specificity and product purity.

153 nt concern that toxicants such as ddC impair mtDNA maintenance in both proliferating and nonprolifera

154 SSBP1 mutations impaired mtDNA, nucleoids, and 7S-DNA amounts as well as mtDNA re

155 s mtDNA is lost from metabolically impaired, mtDNA-intact (rho+) cells.

156 ecies of mitochondrial (mt-)tRNAs encoded in mtDNA translate essential subunits of the respiratory ch

157 cant mean increase of 48.2- and 86.1-fold in mtDNA based on quantitative PCR, and proportion of subse

158 No further increase in mtDNA copy number was observed upon depletion of Pim1 in

159 se deletion resulted in a marked increase in mtDNA levels, while maintaining wild type-like mitochond

160 nding protein, a crucial protein involved in mtDNA replication.

161 Under hypoxia, the 6mA level in mtDNA could be further elevated, suggesting regulatory r

162 and the discovery of pathogenic mutations in mtDNA more than 30 years ago, a movement towards generat

163 ool capable of installing point mutations in mtDNA, and it does not involve CRISPR.

164 newly introduced mtDNA is stably retained in mtDNA-deficient (rho0) recipient cells following uridine

165 w that the Balbiani body has a minor role in mtDNA selective inheritance by supplying healthy mitocho

166 that Huntington's disease mice had increased mtDNA release, cGAS activation, and inflammation, all in

167 tion, affects mtDNA replication, and induces mtDNA depletion.

168 Interestingly, mtDNA biogenesis is not sufficient for this proliferatio

169 mpanied with foveopathy brings insights into mtDNA maintenance disorders.

170 We show that newly introduced mtDNA is stably retained in mtDNA-deficient (rho0) recip

171 ls exposed to 12 muM ddC contained even less mtDNA.

172 c.) significantly affect levels of leukocyte mtDNA copy number in Mexican Americans.

173 effect of the built environment on leukocyte mtDNA copy number has not been studied previously.

174 ents of the built environment with leukocyte mtDNA copy number among 5,502 Mexican American adults en

175 quantitative analysis of three primary LHON mtDNA mutations, offering a promising approach for genet

176 and easy to handle advantages for three LHON mtDNA mutations are rarely reported.

177 tive and quantitative analyses of three LHON mtDNA mutations.

178 PCR for qualitative genotyping of three LHON mtDNA mutations.

179 yers which mediate the degradation of linear mtDNA fragments and possible mechanisms of recirculariza

180 Linking mtDNA sequence features, through this molecular mechanis

181 Lophophytum mtDNA has experienced an unprecedented level of function

182 the study population was stratified into low mtDNA copy number group (< median) and high mtDNA copy n

183 istinct waves, each corresponding to a major mtDNA lineage.

184 ls DNA 6mA as a regulatory mark in mammalian mtDNA.

185 elopments in the transformation of mammalian mtDNA have stood still for some time, recent demonstrati

186 However, recipient cells with matched mtDNA-nDNA failed to retain transferred mtDNA and sustai

187 ive mammalian methyltransferase, can mediate mtDNA 6mA methylation, which contributes to attenuated m

188 mismatched nuclear (nDNA) and mitochondrial (mtDNA) genomes retained transferred mtDNA, which replace

189 l mystery that may pose challenges to modern mtDNA disease therapies, leading to substantial recent a

190 Most, if not all, humans contain multiple mtDNA genotypes (heteroplasmy); specific patterns of var

191 mtDNA, which replaced the endogenous mutant mtDNA and improved cell respiration.

192 The proportion of mutant mtDNA varies across patients and among tissues within a

193 this adaptation, rho(0) cells, which have no mtDNA, exhibit increased growth rates and nuclear genome

194 ls contain a mixture of mutant and nonmutant mtDNA (a phenomenon called heteroplasmy).

195 nd transcript levels of nuclear DNA- but not mtDNA-encoded ETC complex subunits in chRCC.

196 Comparison to a more recent O. nubilalis mtDNA assembly from unenriched short-read data analogous

197 Taken together, assessment of mtDNA damage levels may be a sensitive measure of altere

198 o generate a single-cell-resolution atlas of mtDNA content in mammalian tissues was validated.

199 etic analysis confirmed minimal carryover of mtDNA following MST.

200 winkle helicase is an essential component of mtDNA replication.

201 studied as a disease biomarker, comprises of mtDNA located within mitochondria, indicative of mitocho

202 The rNMP content of mtDNA varied greatly across different tissues and was de

203 qPCR assay for the quantitative detection of mtDNA copy number in blood samples.

204 This previously unrecognized disease of mtDNA maintenance implicates SSBP1 mutations as a cause

205 with replication, leading to disruptions of mtDNA and, eventually, optic nerve dysfunction.

206 oth the size and the spatial distribution of mtDNA nucleoids.

207 To explore the potential effects of mtDNA mutations on bone biology, we compared bone microa

208 Reduced efficiency of mtDNA replication was also reproduced in vitro, confirmi

209 ion of mtDNA, rather than the elimination of mtDNA copies that results from its cleavage by targeted

210 cuss the current knowledge about the fate of mtDNA following double-strand breaks, including the mole

211 Here, we survey the frequency of mtDNA horizontal transfer within the canine transmissibl

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

213 of 5-25%, implying biparental inheritance of mtDNA in 0.06% of offspring.

214 chondrial fission, together with the lack of mtDNA replication, segregate mtDNA into individual organ

215 fold increased odds of having high levels of mtDNA copy number (OR = 1.12, 95% CI 1.01, 1.27).

216 fold increased odds of having high levels of mtDNA copy number [Odds ratio (OR) = 1.24, 95% confidenc

217 /intersection ratio) may influence levels of mtDNA copy number in leukocytes in Mexican Americans.

218 Based on the median levels of mtDNA copy number, the study population was stratified i

219 ly affect mtDNA copy number or the levels of mtDNA molecules with deletions or strand breaks in aged

220 ized self-renewing tissues, higher levels of mtDNA were observed in stem/proliferative compartments c

221 es not contribute to the progressive loss of mtDNA quality that occurs as mice age.

222 enerating methods for robust manipulation of mtDNA has ensued, although with relatively few advances

223 nology suggest that clinical manipulation of mtDNA heteroplasmy may be on the horizon for these large

224 As a consequence, manipulation of mtDNA to date has been limited to the targeted destructi

225 ee DdCBEs enable the precise manipulation of mtDNA, rather than the elimination of mtDNA copies that

226 explored the possibility that measurement of mtDNA damage is a "surrogate" for LRRK2 kinase activity

227 Because most measurements of mtDNA use homogenates of complex tissues, little is know

228 The asynchronous mechanism of mtDNA replication predicts that the replication machiner

229 lian cells could generate improved models of mtDNA disease and support future cell-based therapies.

230 Mutations of mtDNA can cause mitochondrial diseases and are implicate

231 Striking zonal patterns of mtDNA levels in the liver reflected the known oxygen ten

232 , quantify, and manipulate the properties of mtDNA within cells.

233 LRRK2 kinase inhibitors, a full reversal of mtDNA damage to healthy control levels was observed and

234 ize our current understanding of the role of mtDNA genetics in relation to human cancers.

235 Manipulation of the amount and sequence of mtDNA within cells is important experimentally and for d

236 Sequencing of mtDNA identified a mutation in the mitochondrial tRNA(Va

237 dings cast light on the origin and spread of mtDNA mutations at multiple scales, from the organelle t

238 e potential to cause significant stalling of mtDNA replication.

239 find no evidence of paternal transmission of mtDNA in humans.

240 que, not only to prevent the transmission of mtDNA mutations, but also as a new potential treatment f

241 s may produce cells where different types of mtDNA coexist in admixed populations.

242 Visualization of mtDNA within cells is a powerful means by which mechanis

243 ve stress induced high mutation frequency on mtDNA can be indirectly caused by oxidation of the mitoc

244 Human impacts on mtDNA diversity were taxon and scale-dependent, and were

245 stigated the effect of incorporated rNMPs on mtDNA stability over the mouse life span and found that

246 In these admixtures, one mtDNA type is often observed to proliferate over another

247 e penetrance and tissue specificity of other mtDNA mutations and highlight the potential role of amin

248 We then combined our mtDNA data with previous data available from South Afric

249 e cryptic mega-NUMTs can resemble paternally mtDNA heteroplasmy, but find no evidence of paternal tra

250 ll variation in heteroplasmy of a pathologic mtDNA variant, which we associate with intra-individual

251 a correlation between whole blood and plasma mtDNA levels, indicating that the relationship between c

252 Together, these defects promote mtDNA leakage into the cytosol and chronic cGAS engageme

253 n therapy for advanced PCa, further promoted mtDNA secretion in cultured epithelia, mice, and PCa pat

254 ecipients depends on the degree of recipient mtDNA-nDNA co-evolution.

255 attenuated mtDNA transcription and a reduced mtDNA copy number.

256 risingly, the cellular mechanisms regulating mtDNA copy number remain poorly understood.

257 Failure to resolve mtDNA breaks leads to mitochondrial dysfunction and affe

258 There was a greater induction of ROS, mtDNA, and nDNA damage with the inclusion of the visible

259 ith the lack of mtDNA replication, segregate mtDNA into individual organelles in the Drosophila early

260 After mtDNA segregation, mtDNA transcription begins, which activates respiration.

261 m accelerating the selection against selfish mtDNA.

262 We find that the proliferation of selfish mtDNA within hosts depends on nutrient status stimulatin

263 delineates environmental effects on selfish mtDNA dynamics at different levels of selection.

264 as a tendency for a higher number of somatic mtDNA variants among the affected twins.

265 The permanent transfer of specific mtDNA sequences into mammalian cells could generate impr

266 quantifying species- and cell-type-specific mtDNA copy number and dynamics in any normal or diseased

267 es, little is known about cell-type-specific mtDNA copy number heterogeneity in normal physiology, ag

268 hosts depends on nutrient status stimulating mtDNA biogenesis in the developing germline.

269 ion due to impaired mitophagy and subsequent mtDNA release in the pathogenesis of PRKN/PINK1-linked P

270 Besides, the O. subterraneum mtDNA was also subjected to additional HGT events from d

271 Increasing evidence suggests that mtDNA mutations are not the results of direct oxidative

272 The mtDNA of O. subterraneum assembles into 54 circular chro

273 The mtDNA within cells is organized into nucleoids within th

274 xel and C3 receptor antagonist disrupted the mtDNA/C3a paracrine loop and restored docetaxel sensitiv

275 To understand how the mtDNA replicase, Pol gamma, can give rise to elevated mu

276 l molecular tool to edit single bases in the mtDNA (Mok et al., 2020).

277 homologs of each foreign gene coexist in the mtDNA and are potentially functional.

278 opose the stability of G-quadruplexes in the mtDNA control region, influencing the balance between tr

279 The analysis of the mtDNA D-loop of 706 chicken samples from Iraq (n = 107),

280 polymerase gamma is a core component of the mtDNA replisome and the only replicative DNA polymerase

281 tracts (totaling almost 100 kb, ~ 14% of the mtDNA), including 12 intact genes, were acquired by HGT

282 over the mouse life span and found that the mtDNA rNMP content increased during early life.

283 cumulation of RNA:DNA hybrids throughout the mtDNA.

284 Therefore, mtDNA expression acts as a stress test for the integrity

285 complex, providing a scaffold linking it to mtDNA.

286 ies of cellular and tissue-wide responses to mtDNA damage and mito-nuclear genome incompatibility.

287 tor mitochondria, suggesting a robustness to mtDNA mutation.

288 g-term retention and function of transferred mtDNA remains unknown.

289 ched mtDNA-nDNA failed to retain transferred mtDNA and sustained impaired respiration.

290 ondrial (mtDNA) genomes retained transferred mtDNA, which replaced the endogenous mutant mtDNA and im

291 ysis of muscle histology and ultrastructure, mtDNA sequencing, and RNA quantification.

292 nging from New Hampshire to Florida and used mtDNA, three nuclear genetic loci, and incorporated Baye

293 We used mtDNA to characterize specimens of T. peregrinus collect

294 The variable mtDNA depletion in cells was reflected in severity of mi

295 g ddC exposures, we measured cell viability, mtDNA copy number, and mitochondrial bioenergetics utili

296 the holoparasite Lophophytum mirabile, whose mtDNA has lost most native genes but contains intact for

297 peutic approach for diseases associated with mtDNA release.

298 nstrate that Mrx6 partially colocalizes with mtDNA within mitochondria and interacts with the conserv

299 d from injured hepatocyte mitochondria (with mtDNA as major active component) directly activate hepat

300 , Australia, and Europe to construct a world mtDNA network of haplotypes.