Auswahl der wissenschaftlichen Literatur zum Thema „MtDNA segregation“
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Zeitschriftenartikel zum Thema "MtDNA segregation"
Takeda, Kumiko, Seiya Takahashi, Akira Onishi, Hirofumi Hanada und Hiroshi Imai. „Replicative Advantage and Tissue-Specific Segregation of RR Mitochondrial DNA Between C57BL/6 and RR Heteroplasmic Mice“. Genetics 155, Nr. 2 (01.06.2000): 777–83. http://dx.doi.org/10.1093/genetics/155.2.777.
Der volle Inhalt der QuelleLechuga-Vieco, Ana Victoria, Ana Latorre-Pellicer, Iain G. Johnston, Gennaro Prota, Uzi Gileadi, Raquel Justo-Méndez, Rebeca Acín-Pérez et al. „Cell identity and nucleo-mitochondrial genetic context modulate OXPHOS performance and determine somatic heteroplasmy dynamics“. Science Advances 6, Nr. 31 (Juli 2020): eaba5345. http://dx.doi.org/10.1126/sciadv.aba5345.
Der volle Inhalt der QuelleRøyrvik, Ellen C., und Iain G. Johnston. „MtDNA sequence features associated with ‘selfish genomes’ predict tissue-specific segregation and reversion“. Nucleic Acids Research 48, Nr. 15 (27.07.2020): 8290–301. http://dx.doi.org/10.1093/nar/gkaa622.
Der volle Inhalt der QuelleTsang, William Y., und Bernard D. Lemire. „Stable heteroplasmy but differential inheritance of a large mitochondrial DNA deletion in nematodes“. Biochemistry and Cell Biology 80, Nr. 5 (01.10.2002): 645–54. http://dx.doi.org/10.1139/o02-135.
Der volle Inhalt der QuelleLing, Feng, Rong Niu, Hideyuki Hatakeyama, Yu-ichi Goto, Takehiko Shibata und Minoru Yoshida. „Reactive oxygen species stimulate mitochondrial allele segregation toward homoplasmy in human cells“. Molecular Biology of the Cell 27, Nr. 10 (15.05.2016): 1684–93. http://dx.doi.org/10.1091/mbc.e15-10-0690.
Der volle Inhalt der QuelleZelenaya-Troitskaya, Olga, Scott M. Newman, Koji Okamoto, Philip S. Perlman und Ronald A. Butow. „Functions of the High Mobility Group Protein, Abf2p, in Mitochondrial DNA Segregation, Recombination and Copy Number in Saccharomyces cerevisiae“. Genetics 148, Nr. 4 (01.04.1998): 1763–76. http://dx.doi.org/10.1093/genetics/148.4.1763.
Der volle Inhalt der QuelleOkamoto, Koji, Philip S. Perlman und 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, Nr. 3 (10.08.1998): 613–23. http://dx.doi.org/10.1083/jcb.142.3.613.
Der volle Inhalt der QuelleMeirelles, Flávio V., und Lawrence C. Smith. „Mitochondrial Genotype Segregation in a Mouse Heteroplasmic Lineage Produced by Embryonic Karyoplast Transplantation“. Genetics 145, Nr. 2 (01.02.1997): 445–51. http://dx.doi.org/10.1093/genetics/145.2.445.
Der volle Inhalt der QuelleClark, A. G., und E. M. Lyckegaard. „Natural selection with nuclear and cytoplasmic transmission. III. Joint analysis of segregation and mtDNA in Drosophila melanogaster.“ Genetics 118, Nr. 3 (01.03.1988): 471–81. http://dx.doi.org/10.1093/genetics/118.3.471.
Der volle Inhalt der QuelleSmith, Lawrence C., Jacob Thundathil und France Filion. „Role of the mitochondrial genome in preimplantation development and assisted reproductive technologies“. Reproduction, Fertility and Development 17, Nr. 2 (2005): 15. http://dx.doi.org/10.1071/rd04084.
Der volle Inhalt der QuelleDissertationen zum Thema "MtDNA segregation"
Battersby, Brendan James. „Genetic basis for MTDNA segregation in a heteroplasmic mouse model“. Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=38462.
Der volle Inhalt der QuelleKubilinskas, Rokas. „MitoTALENs to explore mitochondrial DNA repair and segregation“. Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ014.
Der volle Inhalt der QuelleFor long, the plant mitochondrial genome (mtDNA) was not amenable to manipulation, until recent advancements in genome engineering using Transcription Activator-Like Effector Nucleases (TALEN). In this work I used TALENs specifically targeted to mitochondria (mitoTALENs) to study plant mtDNA repair and segregation. MitoTALEN constructs were transformed into the background of 10 different Arabidopsis thaliana mutant lines, deficient in various factors involved in plant mitochondrial repair by homologous recombination. The resulting lines were analysed by Illumina sequencing and qPCR approaches. In wild type plants, the mtDNA double-strand-break (DSB) induced by MitoTALENs was repaired by homologous recombination, resulting in the replacement of the region containing the DSB by a distal unaffected sequence of the mtDNA, flanked by the same set of repeated sequences. In mutants deficient in repair factors, repair could shift to alternative pathways, such as Single-Strand Annealing (SSA) and Microhomology-mediated recombination (MHMR). Furthermore, in some mutants, the data revealed no evidence of DSB repair, but rather suggested that plants deficient in key repair factors could survive by reconstituting an alternative viable mitochondrial genome, from pre-existing autonomously replicating sub-genomes
Rajasimha, Harsha Karur. „Insights Into Mitochondrial Genetic and Morphologic Dynamics Gained by Stochastic Simulation“. Diss., Virginia Tech, 2007. http://hdl.handle.net/10919/29961.
Der volle Inhalt der QuellePh. D.
Viramontes, Martínez Francisco. „Heteroplasmy in mammal mitochondrial deoxyribonucleic acid“. Thèse, 2011. http://hdl.handle.net/1866/8723.
Der volle Inhalt der QuelleNature has developed strategies to ensure the beginning of life in conditions of homoplasmy, i.e. cells harboring the same mitochondrial DNA (mtDNA). However, novel mtDNA haplotypes can arise by many means during life, leading to heteroplasmy. For instance, mtDNA heteroplasmy can originate artificially through assisted reproductive technologies and naturally by the process of aging. Therefore, this doctoral thesis was divided into two general objectives: Firstly, to analyze the changes in mtDNA heteroplasmy produced by somatic cell nuclear transfer (SCNT) during development from embryos, to fetuses and adult tissues, in cattle. Secondly, to analyze the changes in mtDNA heteroplasmy caused by aging in adult germinal and somatic tissues, during oogenesis and early embryogenesis, and in in vitro culture procedures in mice. In the first series of experiments in cattle, fetal fibroblasts carrying an mtDNA mutation (insertion of 66 bp) were fused to host oocytes carrying wild type mtDNA. The presence of mtDNA from the donor cell was analyzed in 30 SCNT clones at different stages of development: 17-day-old embryos (n=17); 40-day-old fetuses (n=3); 60-day-old fetuses (n=3); one 240 day-old fetus; and 3 post-natal clones (18-24 months). Every individual clone proved to be heteroplasmic and 99% (103/104) of the analyzed tissue samples were heteroplasmic as well. Only the ovary coming from a 240 day old fetus was homoplasmic for the mtDNA of the recipient oocyte. In most (95.2%) of the analyzed tissue samples (99/104) the mean of heteroplasmy was 1.46%. In contrast, one 40-day-old fetus presented high levels of heteroplasmy (20.9%) indicating rare events of donor mtDNA increases. Since most SCNT clones showed heteroplasmy at proportions comparable to the donor mtDNA at the moment of embryo reconstruction, we concluded that heteroplasmy produced by nuclear transfer techniques using somatic cells is due to the neutral segregation of the mtDNA. In the second series of experiments, performed in mice, females of different ages, i.e. young (0-8 months), middle (8-16 months) and old (16-24 months), were synchronized (gonadotropins) and sacrificed to obtain germinal vesicle oocytes, metaphase-II oocytes in vivo and in vitro. Also, 2-cell and blastocyst stage embryos were obtained from young females in vivo and in vitro. Somatic tissues from females of the three age periods were obtained: brain, granulosa, liver and muscle and the effect of aging was measured on fertility. The effects of aging, stage of development and in vitro culture on the heteroplasmy were measured in oocytes and embryos. Also, the effects of aging were measured in somatic and germinal tissues on total copies of mtDNA, percentage of mtDNA common deletion and the expression of three genes: Ndufs4, Mt-nd2 and Mt-nd4. We observed that female fertility in the mouse colony decreases with age. Aging affected mtDNA in somatic tissues but no effect was observed in granulosa, oocytes and embryos. MtDNA deletions increased during the resumption of meiosis and decreased during early embryo development; and culture in vitro did not affect the mtDNA in most germinal tissues. Because we did not find effects of age in most mitochondrial parameters analyzed in oocytes and embryos, we suggest that mtDNA common deletion in germinal tissues is more related with the cellular status of energy production than with the process of aging. Two different sources of mutations in the mtDNA generated in normal or reconstructed oocytes produced different heteroplasmy outcomes at the beginning of embryogenesis. In cattle, artificial heteroplasmy involving a small insertion (66 bp) in the non coding region (D-loop) of the mitochondrial DNA was apparently not harmful to the embryo, allowing persistence of the foreign mtDNA during the different stages of clonal development. In mice, the natural heteroplasmy of a large deletion (4974 bp, common deletion) in the coding region of the mtDNA was apparently harmful to the embryo and, therefore, may have been eliminated to ensure homoplasmy at the beginning of embryonic development.
Buchteile zum Thema "MtDNA segregation"
Enriquez, Jose-Antonio. „Segregation and dynamics of mitochondrial DNA in mammalian cells“. In Genetics of Mitochondrial Disease, 279–94. Oxford University PressOxford, 2003. http://dx.doi.org/10.1093/oso/9780198508656.003.0014.
Der volle Inhalt der QuelleSchon, Eric A. „Rearrangements of mitochondrial DNA“. In Genetics of Mitochondrial Disease, 111–24. Oxford University PressOxford, 2003. http://dx.doi.org/10.1093/oso/9780198508656.003.0006.
Der volle Inhalt der QuelleBurr, Stephen P., und Patrick F. Chinnery. „Heredity and segregation of mtDNA“. In The Human Mitochondrial Genome, 87–107. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-819656-4.00004-8.
Der volle Inhalt der QuelleSpelbrink, Johannes N. „Replication, repair, and recombination of mitochondrial DNA“. In Genetics of Mitochondrial Disease, 3–26. Oxford University PressOxford, 2003. http://dx.doi.org/10.1093/oso/9780198508656.003.0001.
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