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A study of mitochondrial genome transmission in Saccharomyces cerevisiae using the suppressive petite mutationChambers, P. January 1984 (has links)
No description available.
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Evolution of cytoplasmic genomes /Ralph, David Allen January 1986 (has links)
No description available.
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Biochemical, morphological, and physiological studies on the methane oxidizing bacterium, Methylosinus trichosporium, with emphasis on structure, function, and composition of the intracytoplasmic membranes /Weaver, Terry Lee January 1973 (has links)
No description available.
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Cytoplasmic control of ribosome biogenesis /Racevskis, Janis January 1974 (has links)
No description available.
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Cytoplasmic inheritance and virus diseasesTilney-Bassett, Richard A. E. January 1962 (has links)
No description available.
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Possible cytoplasmic inheritance and its effect on the phenotypic variability in Phytophthora megasperma var. sojaeTrombold, David George January 2011 (has links)
Typescript. / Digitized by Kansas Correctional Industries
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Studies on a cytoplasmically transmitted strain difference in response to the teratogen 6-aminonicotinamidePollard, D. Russell (Donald Russell) January 1969 (has links)
No description available.
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Inheritance of peroxisomes in the yeast Yarrowia lipolyticaChang, Jinlan. January 1900 (has links)
Thesis (Ph.D.)--University of Alberta, 2010. / A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosophy, Department of Cell Biology. Title from pdf file main screen (viewed on July 25, 2010). Includes bibliographical references.
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Studies on a cytoplasmically transmitted strain difference in response to the teratogen 6-aminonicotinamidePollard, D. Russell (Donald Russell) January 1969 (has links)
No description available.
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Transferência de citoplasma submetido ao estresse oxidativo como modelo para o estudo da herança de doenças mitocondriais / Transplantation of cytoplasm subjected to oxidative stress as a model for study of mitochondrial disease inheritanceMachado, Thiago Simões 30 September 2014 (has links)
Patologias causadas por mutações no DNA mitocondrial (mtDNA) constituem um importante grupo de doenças genéticas em humanos. Todavia, devido ao desconhecimento dos mecanismos que governam a herança mitocondrial, não existem métodos eficientes que permitam prever ou intervir na herança destas patologias. Estudos recentes indicam que mutações no mtDNA são seletivamente eliminadas na linhagem germinativa. O presente projeto investigou se o embrião é capaz de eliminar mitocôndrias disfuncionais durante o desenvolvimento pré-implantação. Para tanto, zigotos de camundongo foram tratados com clorometil-X-rosamina (MitoTracker Red CMXRos) e fotossensibilizados por 0, 2,5, 5, 10, 20 e 60 s. Houve diminuição da taxa de blastocisto, com bloqueio total do desenvolvimento quando a fotossensibilização foi realizada por período igual ou superior a 20 s. A fotossensibilização também resultou em disfunção mitocondrial, como indicado por diminuição do potencial de membrana mitocondrial. No entanto, a transferência de citoplasma de zigotos NZB/BINJ (NZB) fotossensibilizados por 20 s não afetou o desenvolvimento de embriões C57BL/6 (B6). A quantidade de mtDNA NZB também não diferiu entre os zigotos B6, independente de terem recebido citoplasma exposto ou não à fotossensibilização (30,6% ± 1,73 vs. 30,8% ± 1,73). Porém, a quantidade de mtDNA NZB foi menor (P = 0,008) nos blastocistos que receberam citoplasma fotossensibilizado (31,4% ± 1,43 vs. 24,7% ± 1,43). Como a quantidade total de mtDNA não diferiu entre os grupos, estes resultados sugerem que as mitocôndrias disfuncionais introduzidas foram destruídas. A análise de autofagossomos indicou, no entanto, que as mitocôndrias NZB não foram eliminadas por mitofagia. Diferente do esperado, o cultivo na presença de rapamicina reverteu o efeito causado pela introdução de citoplasma fotossensibilizado, resultando em níveis semelhantes de mtDNA NZB em comparação com os blastocistos que receberam citoplasma não fotossensibilizado. Concluiu-se que o embrião de camundongo é capaz de destruir mitocôndrias disfuncionais durante o desenvolvimento à blastocisto. Novos estudos deverão fornecer evidências adicionais e esclarecer os mecanismos moleculares que fundamentam esses achados. / Pathologies caused by mutations in mitochondrial DNA (mtDNA) represent an important group of genetic diseases in humans. Nonetheless, due to our limited understanding of the molecular mechanisms of mitochondrial inheritance there are no efficient methods to predict or intervene in the inheritance of these diseases. Recent studies indicate that mutations in mtDNA are selectively eliminated in the germline. This project investigated the ability of the embryo to target and eliminate dysfunctional mitochondria during early development. To test that, mouse zygotes were treated with chloromethyl-X-rosamina (MitoTracker Red CMXRos) and photosensitized for 0, 2.5, 5, 10, 20 and 60 s. There was a decrease in the rate of blastocyst development and a developmental arrest when the photosensitization was performed for a period equal to or greater than 20 s. Photosensitization also resulted in mitochondrial dysfunction, as indicated by a decreased of mitochondrial membrane potential. However, cytoplasmic transfer from NZB/BINJ (NZB) zygotes photosensitized for 20 s resulted in no effect on development of C57BL/6 (B6) embryos. The amount of NZB mtDNA introduced also did not differ between B6 zygotes, regardless of whether they received or not photosensitized cytoplasm (30.6% ± 1.73 vs. 30.8 ± 1.73%). On the other hand, the amount of NZB mtDNA was lower (P = 0.008) in the blastocysts receiving photosensitized cytoplasm (31.4% ± 24.7% ± 1.43 vs. 1.43). Since the total amount of mtDNA was not different between the groups, these results suggest that dysfunctional mitochondria introduced by cytoplasmic transfer were destroyed. Analysis of autophagosomes indicated, however, that the NZB mitochondria were not eliminated by mitophagy. Different than expected, culture in the presence of rapamycin reversed the effect caused by introduction of photosensitized cytoplasm, resulting in similar levels of NZB mtDNA compared to blastocysts receiving cytoplasm not photosensitized. It was concluded that the mouse embryo may destroy dysfunctional mitochondria during development into blastocysts. Further studies should provide additional evidence and elucidate the molecular mechanisms underlying these findings.
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