NDLI: Marked replicative advantage of human mtDNA carrying a point mutation that causes the MELAS encephalomyopathy.

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Marked replicative advantage of human mtDNA carrying a point mutation that causes the MELAS encephalomyopathy.

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Marked replicative advantage of human mtDNA carrying a point mutation that causes the MELAS encephalomyopathy.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Hurko, O. Martinuzzi, A. Yoneda, M. Chomyn, A. Attardi, G.
Description	Author Affiliation: Yoneda M ( Division of Biology, California Institute of Technology, Pasadena 91125.);
Abstract	The segregation of mutant and wild-type mtDNA was investigated in transformants constructed by transferring human mitochondria from individuals belonging to four pedigrees with the MELAS encephalomyopathy-associated mtDNA mutation (MELAS is mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) into human mtDNA-less (rho 0) cells. Five of 13 clonal cell lines containing mixtures of wild-type and mutant mtDNAs were found to undergo a rapid shift of their genotype toward the pure mutant type. The other 8 cell lines, which included 6 exhibiting nearly homoplasmic mutant mtDNA, on the contrary, maintained a stable genotype. Subcloning experiments and growth rate measurements clearly indicated that an intracellular replicative advantage of mutant mtDNA was mainly responsible for the dramatic shift toward the mutant genotype observed in the unstable cell lines.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	23
Volume Number	89
Language	English
Publisher	National Academy of Sciences
Publisher Date	1992-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	DNA Replication DNA, Mitochondrial Metabolism Mitochondrial Encephalomyopathies Genetics Cell Division Cells, Cultured Cloning, Molecular In Vitro Techniques Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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