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Artykuły w czasopismach na temat „MtDNA segregation”

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Data publikacji: 31 sierpnia 2024

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1

Takeda, Kumiko, Seiya Takahashi, Akira Onishi, Hirofumi Hanada, and Hiroshi Imai. "Replicative Advantage and Tissue-Specific Segregation of RR Mitochondrial DNA Between C57BL/6 and RR Heteroplasmic Mice." Genetics 155, no. 2 (2000): 777–83. http://dx.doi.org/10.1093/genetics/155.2.777.

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Abstract To investigate the interactions between mtDNA and nuclear genomes, we produced heteroplasmic maternal lineages by transferring the cytoplasts between the embryos of two mouse strains, C57BL/6 (B6) and RR. A total of 43 different nucleotides exist in the displacement-loop (D-loop) region of mtDNA between B6 and RR. Heteroplasmic embryos were reconstructed by electrofusion using a blastomere from a two-cell stage embryo of one strain and an enucleated blastomere from a two-cell stage embryo of the other strain. Equivalent volumes of both types of mtDNAs were detected in blastocyst stage

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Lechuga-Vieco, Ana Victoria, Ana Latorre-Pellicer, Iain G. Johnston, et al. "Cell identity and nucleo-mitochondrial genetic context modulate OXPHOS performance and determine somatic heteroplasmy dynamics." Science Advances 6, no. 31 (2020): eaba5345. http://dx.doi.org/10.1126/sciadv.aba5345.

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Heteroplasmy, multiple variants of mitochondrial DNA (mtDNA) in the same cytoplasm, may be naturally generated by mutations but is counteracted by a genetic mtDNA bottleneck during oocyte development. Engineered heteroplasmic mice with nonpathological mtDNA variants reveal a nonrandom tissue-specific mtDNA segregation pattern, with few tissues that do not show segregation. The driving force for this dynamic complex pattern has remained unexplained for decades, challenging our understanding of this fundamental biological problem and hindering clinical planning for inherited diseases. Here, we d

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Røyrvik, Ellen C., and Iain G. Johnston. "MtDNA sequence features associated with ‘selfish genomes’ predict tissue-specific segregation and reversion." Nucleic Acids Research 48, no. 15 (2020): 8290–301. http://dx.doi.org/10.1093/nar/gkaa622.

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Abstract Mitochondrial DNA (mtDNA) encodes cellular machinery vital for cell and organism survival. Mutations, genetic manipulation, and gene therapies may produce cells where different types of mtDNA coexist in admixed populations. In these admixtures, one mtDNA type is often observed to proliferate over another, with different types dominating in different tissues. This ‘segregation bias’ is a long-standing biological mystery that may pose challenges to modern mtDNA disease therapies, leading to substantial recent attention in biological and medical circles. Here, we show how an mtDNA sequen

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Tsang, William Y., and Bernard D. Lemire. "Stable heteroplasmy but differential inheritance of a large mitochondrial DNA deletion in nematodes." Biochemistry and Cell Biology 80, no. 5 (2002): 645–54. http://dx.doi.org/10.1139/o02-135.

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Many human mitochondrial diseases are associated with defects in the mitochondrial DNA (mtDNA). Mutated and wild-type forms of mtDNA often coexist in the same cell in a state called heteroplasmy. Here, we report the isolation of a Caenorhabditis elegans strain bearing the 3.1-kb uaDf5 deletion that removes 11 genes from the mtDNA. The uaDf5 deletion is maternally transmitted and has been maintained for at least 100 generations in a stable heteroplasmic state in which it accounts for ~60% of the mtDNA content of each developmental stage. Heteroplasmy levels vary between individual animals (from

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Ling, Feng, Rong Niu, Hideyuki Hatakeyama, Yu-ichi Goto, Takehiko Shibata, and Minoru Yoshida. "Reactive oxygen species stimulate mitochondrial allele segregation toward homoplasmy in human cells." Molecular Biology of the Cell 27, no. 10 (2016): 1684–93. http://dx.doi.org/10.1091/mbc.e15-10-0690.

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Mitochondria that contain a mixture of mutant and wild-type mitochondrial (mt) DNA copies are heteroplasmic. In humans, homoplasmy is restored during early oogenesis and reprogramming of somatic cells, but the mechanism of mt-allele segregation remains unknown. In budding yeast, homoplasmy is restored by head-to-tail concatemer formation in mother cells by reactive oxygen species (ROS)–induced rolling-circle replication and selective transmission of concatemers to daughter cells, but this mechanism is not obvious in higher eukaryotes. Here, using heteroplasmic m.3243A > G primary fibroblast

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Zelenaya-Troitskaya, Olga, Scott M. Newman, Koji Okamoto, Philip S. Perlman, and Ronald A. Butow. "Functions of the High Mobility Group Protein, Abf2p, in Mitochondrial DNA Segregation, Recombination and Copy Number in Saccharomyces cerevisiae." Genetics 148, no. 4 (1998): 1763–76. http://dx.doi.org/10.1093/genetics/148.4.1763.

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Abstract Previous studies have established that the mitochondrial high mobility group (HMG) protein, Abf2p, of Saccharomyces cerevisiae influences the stability of wild-type (ρ+) mitochondrial DNA (mtDNA) and plays an important role in mtDNA organization. Here we report new functions for Abf2p in mtDNA transactions. We find that in homozygous Δabf2 crosses, the pattern of sorting of mtDNA and mitochondrial matrix protein is altered, and mtDNA recombination is suppressed relative to homozygous ABF2 crosses. Although Abf 2p is known to be required for the maintenance of mtDNA in ρ+ cells growing

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Okamoto, Koji, Philip S. Perlman, and Ronald A. Butow. "The Sorting of Mitochondrial DNA and Mitochondrial Proteins in Zygotes: Preferential Transmission of Mitochondrial DNA to the Medial Bud." Journal of Cell Biology 142, no. 3 (1998): 613–23. http://dx.doi.org/10.1083/jcb.142.3.613.

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Green fluorescent protein (GFP) was used to tag proteins of the mitochondrial matrix, inner, and outer membranes to examine their sorting patterns relative to mtDNA in zygotes of synchronously mated yeast cells in ρ+ × ρ0 crosses. When transiently expressed in one of the haploid parents, each of the marker proteins distributes throughout the fused mitochondrial reticulum of the zygote before equilibration of mtDNA, although the membrane markers equilibrate slower than the matrix marker. A GFP-tagged form of Abf2p, a mtDNA binding protein required for faithful transmission of ρ+ mtDNA in vegeta

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Meirelles, Flávio V., and Lawrence C. Smith. "Mitochondrial Genotype Segregation in a Mouse Heteroplasmic Lineage Produced by Embryonic Karyoplast Transplantation." Genetics 145, no. 2 (1997): 445–51. http://dx.doi.org/10.1093/genetics/145.2.445.

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Mitochondrial genotypes have been shown to segregate both rapidly and slowly when transmitted to consecutive generations in mammals. Our objective was to develop an animal model to analyze the patterns of mammalian mitochondrial DNA (mtDNA) segregation and transmission in an intraspecific heteroplasmic maternal lineage to investigate the mechanisms controlling these phenomena. Heteroplasmic progeny were obtained from reconstructed blastocysts derived by transplantation of pronuclear-stage karyoplasts to enucleated zygotes with different mtDNA. Although the reconstructed zygotes contained on av

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9

Clark, A. G., and E. M. Lyckegaard. "Natural selection with nuclear and cytoplasmic transmission. III. Joint analysis of segregation and mtDNA in Drosophila melanogaster." Genetics 118, no. 3 (1988): 471–81. http://dx.doi.org/10.1093/genetics/118.3.471.

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Abstract Despite the widespread use of mitochondrial DNA by evolutionary geneticists, relatively little effort has been spent assessing the magnitude of forces maintaining mtDNA sequence diversity. In this study the influence of cytoplasmic variation on viability in Drosophila was examined by analysis of second chromosome segregation. A factorial experiment with balancer chromosomes permitted the effects of cytoplasma and reciprocal crosses to be individually distinguished. The first test used six lines of diverse geographic origin, testing the segregation of all six second chromosomes in all

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Smith, Lawrence C., Jacob Thundathil, and France Filion. "Role of the mitochondrial genome in preimplantation development and assisted reproductive technologies." Reproduction, Fertility and Development 17, no. 2 (2005): 15. http://dx.doi.org/10.1071/rd04084.

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Our fascination for mitochondria relates to their origin as symbiotic, semi-independent organisms on which we, as eukaryotic beings, rely nearly exclusively to produce energy for every cell function. Therefore, it is not surprising that these organelles play an essential role in many events during early development and in artificial reproductive technologies (ARTs) applied to humans and domestic animals. However, much needs to be learned about the interactions between the nucleus and the mitochondrial genome (mtDNA), particularly with respect to the control of transcription, replication and se

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Meeusen, Shelly, Quinton Tieu, Edith Wong, et al. "Mgm101p Is a Novel Component of the Mitochondrial Nucleoid That Binds DNA and Is Required for the Repair of Oxidatively Damaged Mitochondrial DNA." Journal of Cell Biology 145, no. 2 (1999): 291–304. http://dx.doi.org/10.1083/jcb.145.2.291.

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Maintenance of mitochondrial DNA (mtDNA) during cell division is required for progeny to be respiratory competent. Maintenance involves the replication, repair, assembly, segregation, and partitioning of the mitochondrial nucleoid. MGM101 has been identified as a gene essential for mtDNA maintenance in S. cerevisiae, but its role is unknown. Using liquid chromatography coupled with tandem mass spectrometry, we identified Mgm101p as a component of highly enriched nucleoids, suggesting that it plays a nucleoid-specific role in maintenance. Subcellular fractionation, indirect immunofluorescence a

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12

Ling, Feng, and Takehiko Shibata. "Mhr1p-dependent Concatemeric Mitochondrial DNA Formation for Generating Yeast Mitochondrial Homoplasmic Cells." Molecular Biology of the Cell 15, no. 1 (2004): 310–22. http://dx.doi.org/10.1091/mbc.e03-07-0508.

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Mitochondria carry many copies of mitochondrial DNA (mtDNA), but mt-alleles quickly segregate during mitotic growth through unknown mechanisms. Consequently, all mtDNA copies are often genetically homogeneous within each individual (“homoplasmic”). Our previous study suggested that tandem multimers (“concatemers”) formed mainly by the Mhr1p (a yeast nuclear gene-encoded mtDNA-recombination protein)-dependent pathway are required for mtDNA partitioning into buds with concomitant monomerization. The transmission of a few randomly selected clones (as concatemers) of mtDNA into buds is a possible

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Goffart, Steffi, Anu Hangas, and Jaakko L. O. Pohjoismäki. "Twist and Turn—Topoisomerase Functions in Mitochondrial DNA Maintenance." International Journal of Molecular Sciences 20, no. 8 (2019): 2041. http://dx.doi.org/10.3390/ijms20082041.

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Like any genome, mitochondrial DNA (mtDNA) also requires the action of topoisomerases to resolve topological problems in its maintenance, but for a long time, little was known about mitochondrial topoisomerases. The last years have brought a closer insight into the function of these fascinating enzymes in mtDNA topology regulation, replication, transcription, and segregation. Here, we summarize the current knowledge about mitochondrial topoisomerases, paying special attention to mammalian mitochondrial genome maintenance. We also discuss the open gaps in the existing knowledge of mtDNA topolog

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Luo, Shiyu, C. Alexander Valencia, Jinglan Zhang, et al. "Biparental Inheritance of Mitochondrial DNA in Humans." Proceedings of the National Academy of Sciences 115, no. 51 (2018): 13039–44. http://dx.doi.org/10.1073/pnas.1810946115.

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Although there has been considerable debate about whether paternal mitochondrial DNA (mtDNA) transmission may coexist with maternal transmission of mtDNA, it is generally believed that mitochondria and mtDNA are exclusively maternally inherited in humans. Here, we identified three unrelated multigeneration families with a high level of mtDNA heteroplasmy (ranging from 24 to 76%) in a total of 17 individuals. Heteroplasmy of mtDNA was independently examined by high-depth whole mtDNA sequencing analysis in our research laboratory and in two Clinical Laboratory Improvement Amendments and College

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Cao, Liqin, Ellen Kenchington, and Eleftherios Zouros. "Differential Segregation Patterns of Sperm Mitochondria in Embryos of the Blue Mussel (Mytilus edulis)." Genetics 166, no. 2 (2004): 883–94. http://dx.doi.org/10.1093/genetics/166.2.883.

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Abstract In Mytilus, females carry predominantly maternal mitochondrial DNA (mtDNA) but males carry maternal mtDNA in their somatic tissues and paternal mtDNA in their gonads. This phenomenon, known as doubly uniparental inheritance (DUI) of mtDNA, presents a major departure from the uniparental transmission of organelle genomes. Eggs of Mytilus edulis from females that produce exclusively daughters and from females that produce mostly sons were fertilized with sperm stained with MitoTracker Green FM, allowing observation of sperm mitochondria in the embryo by epifluorescent and confocal micro

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Moreira, Jesse D., Deepa M. Gopal, Darrell N. Kotton, and Jessica L. Fetterman. "Gaining Insight into Mitochondrial Genetic Variation and Downstream Pathophysiology: What Can i(PSCs) Do?" Genes 12, no. 11 (2021): 1668. http://dx.doi.org/10.3390/genes12111668.

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Mitochondria are specialized organelles involved in energy production that have retained their own genome throughout evolutionary history. The mitochondrial genome (mtDNA) is maternally inherited and requires coordinated regulation with nuclear genes to produce functional enzyme complexes that drive energy production. Each mitochondrion contains 5–10 copies of mtDNA and consequently, each cell has several hundreds to thousands of mtDNAs. Due to the presence of multiple copies of mtDNA in a mitochondrion, mtDNAs with different variants may co-exist, a condition called heteroplasmy. Heteroplasmi

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Chomyn, A., G. Meola, N. Bresolin, S. T. Lai, G. Scarlato, and G. Attardi. "In vitro genetic transfer of protein synthesis and respiration defects to mitochondrial DNA-less cells with myopathy-patient mitochondria." Molecular and Cellular Biology 11, no. 4 (1991): 2236–44. http://dx.doi.org/10.1128/mcb.11.4.2236-2244.1991.

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A severe mitochondrial protein synthesis defect in myoblasts from a patient with mitochondrial myopathy was transferred with myoblast mitochondria into two genetically unrelated mitochondrial DNA (mtDNA)-less human cell lines, pointing to an mtDNA alteration as being responsible and sufficient for causing the disease. The transfer of the defect correlated with marked deficiencies in respiration and cytochrome c oxidase activity of the transformants and the presence in their mitochondria of mtDNA carrying a tRNA(Lys) mutation. Furthermore, apparently complete segregation of the defective genoty

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Chomyn, A., G. Meola, N. Bresolin, S. T. Lai, G. Scarlato, and G. Attardi. "In vitro genetic transfer of protein synthesis and respiration defects to mitochondrial DNA-less cells with myopathy-patient mitochondria." Molecular and Cellular Biology 11, no. 4 (1991): 2236–44. http://dx.doi.org/10.1128/mcb.11.4.2236.

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A severe mitochondrial protein synthesis defect in myoblasts from a patient with mitochondrial myopathy was transferred with myoblast mitochondria into two genetically unrelated mitochondrial DNA (mtDNA)-less human cell lines, pointing to an mtDNA alteration as being responsible and sufficient for causing the disease. The transfer of the defect correlated with marked deficiencies in respiration and cytochrome c oxidase activity of the transformants and the presence in their mitochondria of mtDNA carrying a tRNA(Lys) mutation. Furthermore, apparently complete segregation of the defective genoty

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Vachin, Pauline, Elodie Adda-Herzog, Gihad Chalouhi, et al. "Segregation of mitochondrial DNA mutations in the human placenta: implication for prenatal diagnosis of mtDNA disorders." Journal of Medical Genetics 55, no. 2 (2017): 131–36. http://dx.doi.org/10.1136/jmedgenet-2017-104615.

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BackgroundMitochondrial DNA (mtDNA) disorders have a high clinical variability, mainly explained by variation of the mutant load across tissues. The high recurrence risk of these serious diseases commonly results in requests from at-risk couples for prenatal diagnosis (PND), based on determination of the mutant load on a chorionic villous sample (CVS). Such procedures are hampered by the lack of data regarding mtDNA segregation in the placenta.The objectives of this report were to determine whether mutant loads (1) are homogeneously distributed across the whole placentas, (2) correlate with th

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Shitara, Hiroshi, Jun-Ichi Hayashi, Sumiyo Takahama, Hideki Kaneda, and Hiromichi Yonekawa. "Maternal Inheritance of Mouse mtDNA in Interspecific Hybrids: Segregation of the Leaked Paternal mtDNA Followed by the Prevention of Subsequent Paternal Leakage." Genetics 148, no. 2 (1998): 851–57. http://dx.doi.org/10.1093/genetics/148.2.851.

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Abstract The transmission profiles of sperm mtDNA introduced into fertilized eggs were examined in detail in F1 hybrids of mouse interspecific crosses by addressing three aspects. The first is whether the leaked paternal mtDNA in fertilized eggs produced by interspecific crosses was distributed stably to all tissues after the eggs' development to adults. The second is whether the leaked paternal mtDNA was transmitted to the subsequent generations. The third is whether paternal mtDNA continuously leaks in subsequent backcrosses. For identification of the leaked paternal mtDNA, we prepared total

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Yamada, Mitsutoshi, Kazuhiro Akashi, Reina Ooka, Kenji Miyado, and Hidenori Akutsu. "Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes." International Journal of Molecular Sciences 21, no. 16 (2020): 5880. http://dx.doi.org/10.3390/ijms21165880.

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Mitochondria are energy-producing intracellular organelles containing their own genetic material in the form of mitochondrial DNA (mtDNA), which codes for proteins and RNAs essential for mitochondrial function. Some mtDNA mutations can cause mitochondria-related diseases. Mitochondrial diseases are a heterogeneous group of inherited disorders with no cure, in which mutated mtDNA is passed from mothers to offspring via maternal egg cytoplasm. Mitochondrial replacement (MR) is a genome transfer technology in which mtDNA carrying disease-related mutations is replaced by presumably disease-free mt

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Cupini, L. M., R. Massa, R. Floris, et al. "Migraine-like disorder segregating with mtDNA 14484 Leber hereditary optic neuropathy mutation." Neurology 60, no. 4 (2003): 717–19. http://dx.doi.org/10.1212/01.wnl.0000048662.77572.fb.

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The authors report neurologic features in a large family harboring the mitochondrial DNA (mtDNA) mutation T14484C associated with Leber hereditary optic neuropathy (LHON). In the maternal line the mtDNA mutation was associated with optic neuropathy or migraine with aura or without aura and transient neurologic/visual disturbances. The segregation of familiar cases of migraine and LHON mutation broadens the clinical phenotype associated with a primary LHON mutation.

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Pickrell, Alicia M., and Richard J. Youle. "Mitochondrial Disease: mtDNA and Protein Segregation Mysteries in iPSCs." Current Biology 23, no. 23 (2013): R1052—R1054. http://dx.doi.org/10.1016/j.cub.2013.10.048.

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Boldogh, Istvan R., Dan W. Nowakowski, Hyeong-Cheol Yang, et al. "A Protein Complex Containing Mdm10p, Mdm12p, and Mmm1p Links Mitochondrial Membranes and DNA to the Cytoskeleton-based Segregation Machinery." Molecular Biology of the Cell 14, no. 11 (2003): 4618–27. http://dx.doi.org/10.1091/mbc.e03-04-0225.

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Previous studies indicate that two proteins, Mmm1p and Mdm10p, are required to link mitochondria to the actin cytoskeleton of yeast and for actin-based control of mitochondrial movement, inheritance and morphology. Both proteins are integral mitochondrial outer membrane proteins. Mmm1p localizes to punctate structures in close proximity to mitochondrial DNA (mtDNA) nucleoids. We found that Mmm1p and Mdm10p exist in a complex with Mdm12p, another integral mitochondrial outer membrane protein required for mitochondrial morphology and inheritance. This interpretation is based on observations that

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Bastiaans, E., D. K. Aanen, A. J. M. Debets, R. F. Hoekstra, B. Lestrade, and M. F. P. M. Maas. "Regular bottlenecks and restrictions to somatic fusion prevent the accumulation of mitochondrial defects in Neurospora." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1646 (2014): 20130448. http://dx.doi.org/10.1098/rstb.2013.0448.

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The replication and segregation of multi-copy mitochondrial DNA (mtDNA) are not under strict control of the nuclear DNA. Within-cell selection may thus favour variants with an intracellular selective advantage but a detrimental effect on cell fitness. High relatedness among the mtDNA variants of an individual is predicted to disfavour such deleterious selfish genetic elements, but experimental evidence for this hypothesis is scarce. We studied the effect of mtDNA relatedness on the opportunities for suppressive mtDNA variants in the fungus Neurospora carrying the mitochondrial mutator plasmid

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Lehtinen, Sanna K., Nicole Hance, Abdellatif El Meziane, et al. "Genotypic Stability, Segregation and Selection in Heteroplasmic Human Cell Lines Containing np 3243 Mutant mtDNA." Genetics 154, no. 1 (2000): 363–80. http://dx.doi.org/10.1093/genetics/154.1.363.

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Abstract The mitochondrial genotype of heteroplasmic human cell lines containing the pathological np 3243 mtDNA mutation, plus or minus its suppressor at np 12300, has been followed over long periods in culture. Cell lines containing various different proportions of mutant mtDNA remained generally at a consistent, average heteroplasmy value over at least 30 wk of culture in nonselective media and exhibited minimal mitotic segregation, with a segregation number comparable with mtDNA copy number (≥1000). Growth in selective medium of cells at 99% np 3243 mutant mtDNA did, however, allow the isol

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Vozáriková, Veronika, Nina Kunová, Jacob A. Bauer, et al. "Mitochondrial HMG-Box Containing Proteins: From Biochemical Properties to the Roles in Human Diseases." Biomolecules 10, no. 8 (2020): 1193. http://dx.doi.org/10.3390/biom10081193.

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Mitochondrial DNA (mtDNA) molecules are packaged into compact nucleo-protein structures called mitochondrial nucleoids (mt-nucleoids). Their compaction is mediated in part by high-mobility group (HMG)-box containing proteins (mtHMG proteins), whose additional roles include the protection of mtDNA against damage, the regulation of gene expression and the segregation of mtDNA into daughter organelles. The molecular mechanisms underlying these functions have been identified through extensive biochemical, genetic, and structural studies, particularly on yeast (Abf2) and mammalian mitochondrial tra

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Ling, Feng, Akiko Hori, and Takehiko Shibata. "DNA Recombination-Initiation Plays a Role in the Extremely Biased Inheritance of Yeast [rho−] Mitochondrial DNA That Contains the Replication Origin ori5." Molecular and Cellular Biology 27, no. 3 (2006): 1133–45. http://dx.doi.org/10.1128/mcb.00770-06.

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ABSTRACT Hypersuppressiveness, as observed in Saccharomyces cerevisiae, is an extremely biased inheritance of a small mitochondrial DNA (mtDNA) fragment that contains a replication origin (HS [rho −] mtDNA). Our previous studies showed that concatemers (linear head-to-tail multimers) are obligatory intermediates for mtDNA partitioning and are primarily formed by rolling-circle replication mediated by Mhr1, a protein required for homologous mtDNA recombination. In this study, we found that Mhr1 is required for the hypersuppressiveness of HS [ori5] [rho −] mtDNA harboring ori5, one of the replic

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Satta, Yoko, Nobue Toyohara, Chiaki Ohtaka, et al. "Dubious maternal inheritance of mitochondrial DNA in D. simulans and evolution of D. mauritiana." Genetical Research 52, no. 1 (1988): 1–6. http://dx.doi.org/10.1017/s0016672300027245.

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SummaryWithin-line heterogeneity has been found in the mitochondrial DNA (mtDNA) in two isofemale lines of D. simulans. The co-existing types, S and M, were typical of the mtDNA in D. simulans and in D. mauritiana, respectively, their nucleotide divergence per site being ca. 2·1%. Segregation analysis confirmed that some individuals in these lines were heteroplasmic and suggested incomplete maternal inheritance of mtDNA in Drosophila. Examination of other lines of D. simulans revealed that the M type of D. mauritiana occurs at 71% in Réunion, 38% in Madagascar and 0% in Kenya. This finding and

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Kauppila, Timo E. S., Ana Bratic, Martin Borch Jensen, et al. "Mutations of mitochondrial DNA are not major contributors to aging of fruit flies." Proceedings of the National Academy of Sciences 115, no. 41 (2018): E9620—E9629. http://dx.doi.org/10.1073/pnas.1721683115.

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Mammals develop age-associated clonal expansion of somatic mtDNA mutations resulting in severe respiratory chain deficiency in a subset of cells in a variety of tissues. Both mathematical modeling based on descriptive data from humans and experimental data from mtDNA mutator mice suggest that the somatic mutations are formed early in life and then undergo mitotic segregation during adult life to reach very high levels in certain cells. To address whether mtDNA mutations have a universal effect on aging metazoans, we investigated their role in physiology and aging of fruit flies. To this end, w

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Kaufman, Brett A., Nela Durisic, Jeffrey M. Mativetsky, et al. "The Mitochondrial Transcription Factor TFAM Coordinates the Assembly of Multiple DNA Molecules into Nucleoid-like Structures." Molecular Biology of the Cell 18, no. 9 (2007): 3225–36. http://dx.doi.org/10.1091/mbc.e07-05-0404.

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Packaging DNA into condensed structures is integral to the transmission of genomes. The mammalian mitochondrial genome (mtDNA) is a high copy, maternally inherited genome in which mutations cause a variety of multisystem disorders. In all eukaryotic cells, multiple mtDNAs are packaged with protein into spheroid bodies called nucleoids, which are the fundamental units of mtDNA segregation. The mechanism of nucleoid formation, however, remains unknown. Here, we show that the mitochondrial transcription factor TFAM, an abundant and highly conserved High Mobility Group box protein, binds DNA coope

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Viramontes, F., F. Filion, and L. C. Smith. "5 NEUTRAL SEGREGATION OF DONOR CELL MITOCHONDRIA IN FETAL AND ADULT TISSUES OF SOMATIC CELL CLONES IN CATTLE." Reproduction, Fertility and Development 17, no. 2 (2005): 153. http://dx.doi.org/10.1071/rdv17n2ab5.

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Until now, animal cloning has been extremely inefficient: only 1–2% of nuclear transfer (NT) clones survive to birth. Some of these anomalies may be related to an incompatibility between nuclear and mitochondrial genes (Cummins JM 2001 Hum. Reprod. Update 7, 217–228). Controversy exists as to the levels of donor cell mitochondrial DNA (mtDNA) inheritance in somatic clones (heteroplasmy). Whereas some researchers found very low quantities (0.1–4%) (Steinborn R et al. 2000 Nat. Genet. 25, 255–257), others found levels of heteroplasmy ranging from 6 to 40% (Takeda et al. Mol. Reprod. Dev. 64, 429

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Battersby, Brendan J., and Eric A. Shoubridge. "Reactive oxygen species and the segregation of mtDNA sequence variants." Nature Genetics 39, no. 5 (2007): 571–72. http://dx.doi.org/10.1038/ng0507-571.

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Kurtz, Andreas, Maria Lueth, Lan Kluwe, et al. "Somatic Mitochondrial DNA Mutations in Neurofibromatosis Type 1-Associated Tumors." Molecular Cancer Research 2, no. 8 (2004): 433–41. http://dx.doi.org/10.1158/1541-7786.433.2.8.

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Abstract Neurofibromatosis type 1 is an autosomal dominantly inherited disease predisposing to a multitude of tumors, most characteristically benign plexiform neurofibromas and diffuse cutaneous neurofibromas. We investigated the presence and distribution of somatic mitochondrial DNA (mtDNA) mutations in neurofibromas and in nontumor tissue of neurofibromatosis type 1 patients. MtDNA alterations in the entire mitochondrial genome were analyzed by temporal temperature gradient gel electrophoresis followed by DNA sequencing. Somatic mtDNA mutations in tumors were found in 7 of 19 individuals wit

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Cieslak, Jakub, Lukasz Wodas, Alicja Borowska, Ernest G. Cothran, Anas M. Khanshour, and Mariusz Mackowski. "Characterization of the Polish Primitive Horse (Konik) maternal lines using mitochondrial D-loop sequence variation." PeerJ 5 (August 24, 2017): e3714. http://dx.doi.org/10.7717/peerj.3714.

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The Polish Primitive Horse (PPH, Konik) is a Polish native horse breed managed through a conservation program mainly due to its characteristic phenotype of a primitive horse. One of the most important goals of PPH breeding strategy is the preservation and equal development of all existing maternal lines. However, until now there was no investigation into the real genetic diversity of 16 recognized PPH dam lines using mtDNA sequence variation. Herein, we describe the phylogenetic relationships between the PPH maternal lines based upon partial mtDNA D-loop sequencing of 173 individuals. Altogeth

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DiMauro, Salvatore. "A Brief History of Mitochondrial Pathologies." International Journal of Molecular Sciences 20, no. 22 (2019): 5643. http://dx.doi.org/10.3390/ijms20225643.

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The history of “mitochondrial pathologies”, namely genetic pathologies affecting mitochondrial metabolism because of mutations in nuclear DNA-encoded genes for proteins active inside mitochondria or mutations in mitochondrial DNA-encoded genes, began in 1988. In that year, two different groups of researchers discovered, respectively, large-scale single deletions of mitochondrial DNA (mtDNA) in muscle biopsies from patients with “mitochondrial myopathies” and a point mutation in the mtDNA gene for subunit 4 of NADH dehydrogenase (MTND4), associated with maternally inherited Leber’s hereditary o

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Adel Hussein, Marwa, Ruaa Hameed Abdulridha, Ibtisam Jasim Sodan, et al. "Mitochondrial DNA and Disease: A review." Al-Nahrain Journal of Science 27, no. 2 (2024): 81–90. http://dx.doi.org/10.22401/anjs.27.2.08.

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Mitochondria are organelles responsible for converting energy into a usable form for cellular metabolic activities. These organelles have their own DNA. Mutations in mitochondrial DNA (mtDNA) are frequent despite Its limited number of genes. Molecular genetics diagnostics enables the examination of DNA in manyfields,like infectiology, cancer, andgenetics of people. It is essential to identify abnormalities in mitochondrial DNA in patients since these mutations directly affect mitochondrial metabolism and may contribute to various illnesses. The mtDNA found in every human cell is a limited and

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Poulton, J. "Segregation of mitochondrial DNA (mtDNA) in human oocytes and in animal models of mtDNA disease: clinical implications." Reproduction 123, no. 6 (2002): 751–55. http://dx.doi.org/10.1530/reprod/123.6.751.

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Yin, Tao, Jikun Wang, Hai Xiang, Carl A. Pinkert, Qiuyan Li, and Xingbo Zhao. "Dynamic characteristics of the mitochondrial genome in SCNT pigs." Biological Chemistry 400, no. 5 (2019): 613–23. http://dx.doi.org/10.1515/hsz-2018-0273.

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Abstract Most animals generated by somatic cell nuclear transfer (SCNT) are heteroplasmic; inheriting mitochondrial genetics from both donor cells and recipient oocytes. However, the mitochondrial genome and functional mitochondrial gene expression in SCNT animals are rarely studied. Here, we report the production of SCNT pigs to study introduction, segregation, persistence and heritability of mitochondrial DNA transfer during the SCNT process. Porcine embryonic fibroblast cells from male and female Xiang pigs were transferred into enucleated oocytes from Yorkshire or Landrace pigs. Ear biopsi

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Nunnari, J., W. F. Marshall, A. Straight, A. Murray, J. W. Sedat, and P. Walter. "Mitochondrial transmission during mating in Saccharomyces cerevisiae is determined by mitochondrial fusion and fission and the intramitochondrial segregation of mitochondrial DNA." Molecular Biology of the Cell 8, no. 7 (1997): 1233–42. http://dx.doi.org/10.1091/mbc.8.7.1233.

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To gain insight into the process of mitochondrial transmission in yeast, we directly labeled mitochondrial proteins and mitochondrial DNA (mtDNA) and observed their fate after the fusion of two cells. To this end, mitochondrial proteins in haploid cells of opposite mating type were labeled with different fluorescent dyes and observed by fluorescence microscopy after mating of the cells. Parental mitochondrial protein markers rapidly redistributed and colocalized throughout zygotes, indicating that during mating, parental mitochondria fuse and their protein contents intermix, consistent with re

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Saavedra, Carlos, Donald T. Stewart, Rebecca R. Stanwood, and Eleftherios Zouros. "Species-Specific Segregation of Gender-Associated Mitochondrial DNA Types in an Area Where Two Mussel Species (Mytilus edulis and M. trossulus) Hybridize." Genetics 143, no. 3 (1996): 1359–67. http://dx.doi.org/10.1093/genetics/143.3.1359.

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Abstract In each of the mussel species Mytilus edulis and M. trossulus there exist two types of mtDNA, the F type transmitted through females and the M type transmitted through males. Because the two species produce fertile hybrids in nature, F and M types of one may introgress into the other. We present the results from a survey of a population in which extensive hybridization occurs between these two species. Among specimens classified as “pure” M. edulis or “pure” M. trossulus on the basis of allozyme analysis, we observed no animal that carried the F or the M mitotype of the other species.

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Nicholls, Thomas J., Cristina A. Nadalutti, Elisa Motori та ін. "Topoisomerase 3α Is Required for Decatenation and Segregation of Human mtDNA". Molecular Cell 69, № 1 (2018): 9–23. http://dx.doi.org/10.1016/j.molcel.2017.11.033.

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Jokinen⁎, Riikka, Paula Marttinen, Katarin Sandell, et al. "Cloning a novel mitochondrial protein which regulates tissue-specific mtDNA segregation." Mitochondrion 11, no. 4 (2011): 641–42. http://dx.doi.org/10.1016/j.mito.2011.03.023.

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Howell, Neil, Soumitra S. Ghosh, Eoin Fahy, and Laurence A. Bindoff. "Longitudinal analysis of the segregation of mtDNA mutations in heteroplasmic individuals." Journal of the Neurological Sciences 172, no. 1 (2000): 1–6. http://dx.doi.org/10.1016/s0022-510x(99)00207-5.

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Tesarova, M., H. Hansikova, J. Kytnarova, et al. "Clinical Heterogeneity, Tissue Distribution, and Intergenerational Segregation of mtDNA Mutation A3243G." Toxicology Mechanisms and Methods 14, no. 1-2 (2004): 79–84. http://dx.doi.org/10.1080/15376520490257527.

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Aretz, Ina, Christopher Jakubke, and Christof Osman. "Power to the daughters – mitochondrial and mtDNA transmission during cell division." Biological Chemistry 401, no. 5 (2020): 533–46. http://dx.doi.org/10.1515/hsz-2019-0337.

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AbstractMitochondria supply virtually all eukaryotic cells with energy through ATP production by oxidative phosphoryplation (OXPHOS). Accordingly, maintenance of mitochondrial function is fundamentally important to sustain cellular health and various diseases have been linked to mitochondrial dysfunction. Biogenesis of OXPHOS complexes crucially depends on mitochondrial DNA (mtDNA) that encodes essential subunits of the respiratory chain and is distributed in multiple copies throughout the mitochondrial network. During cell division, mitochondria, including mtDNA, need to be accurately apporti

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Kustova, Maria E., Vasilina A. Sokolova, Oksana V. Kidgotko, Mikhail G. Bass, Faina M. Zakharova, and Vadim B. Vasilyev. "Distribution of introduced human mitochondrial DNA in early stage mouse embryos." Medical academic journal 20, no. 2 (2020): 69–78. http://dx.doi.org/10.17816/maj34657.

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Objective. The aim of study was the analysis of human mitochondrial DNA (mtDNA) distribution among murine blastomeres in the embryos developing after an injection of human mitochondria suspension at the stage of one or two cells is presented. Material and methods. Mice CBA/C57Black from Rappolovo aged three weeks were used. Zygotes were obtained upon hormonal stimulation of animals and mated with males. 310 pL of mitochondrial suspension from HepG2 cells was injected into a zygote or one blastomere of a two-cell embryo. Zygotes or two-cell embryos cultured in M3 medium drops covered with

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Blok, Rozanne B., Debra A. Gook, David R. Thorburn, and Hans-Henrik M. Dahl. "Skewed Segregation of the mtDNA nt 8993 (TrG) Mutation in Human Oocytes." American Journal of Human Genetics 60, no. 6 (1997): 1495–501. http://dx.doi.org/10.1086/515453.

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Cavelier, Lucia, Elena Jazin, Paula Jalonen, and Ulf Gyllensten. "MtDNA substitution rate and segregation of heteroplasmy in coding and noncoding regions." Human Genetics 107, no. 1 (2000): 45–50. http://dx.doi.org/10.1007/s004390000305.

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Cavelier, Lucia, Elena Jazin, Paula Jalonen, and Ulf Gyllensten. "MtDNA substitution rate and segregation of heteroplasmy in coding and noncoding regions." Human Genetics 107, no. 1 (2000): 45–50. http://dx.doi.org/10.1007/s004390050009.

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