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Genetics of aging

Database
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.

Stress resistance, genetic manipulations prolonging life span

One of Dr. R. J. Shmookler Reis’s research areas is the search of genes regulating life span of nematode Caenorhabditis elegans. Shmookler Reis’s laboratory has created mutant nematodes that have age-1 gene with truncated phosphatidylinositol 3-kinase catalytic subunit (PI3KCS). Such PI3KCS mutants have had remarkable longevity. They also have had prolonged period of development and normal mobility. On the other hand, C. elegans PI3KCS mutants have sacrificed their body size and metabolic rate. Such worms have also had exceptional resistance to oxidative and electrophilic stress as compared to worms with normal alleles or alleles associated with lesser life spans. Mutant worms have lived 145–190 days at 20 degrees centigrade showing ten times extension of average and maximum life span.