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Features of mitochondrial aging

In the laboratory headed by K. Khrapko, particular interest is paid to the role of mtDNA somatic mutations in human aging. Scientists investigate the amount of mtDNA mutations in individual cells. Using such approach — evaluating the amount of mtDNA mutations in individual cells — it was found that the level of mtDNA deletions in human pigmented neurons was very high. Among other research guidelines of the laboratory, there are studies focused on mtDNA recombination and studies of mtDNA using microarrays. It is generally assumed that mtDNA mutations are created in the cells where those mutations are currently found. However, it was shown that cells with a particular mtDNA mutation tended to «cluster». Cells of those clusters are usually descendants of the single sell. Thus, mutations in mtDNA do not appear the cells of a cluster, but in progenitor cells, such as stem cells, or even earlier in the development. MtDNA mutatios in progenitor cells may be one of the major sources of mtDNA mutations in healthy aging tissue.

Place of employment — Gerontology Division, Beth Israel Deaconess Medical Center, USA.

Contacts — 330 Brookline Ave; SL-201 Boston, MA 02215, USA(617) 632-0334kkhrapko@bidmc.harvard.edu .

Publications — Quantitative analysis of somatic mitochondrial DNA mutations by single-cell single-molecule PCR. Kraytsberg Y, Bodyak N, Myerow S, Nicholas A, Ebralidze K, Khrapko K. Methods Mol Biol. 2009;554:329–69.Do mtDNA deletions drive premature aging in mtDNA mutator mice? Kraytsberg Y, Simon DK, Turnbull DM, Khrapko K. Aging Cell. 2009 Aug;8(4):502–6. Epub 2009 Apr 22.