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Premature ageing in mice expressing defective mitochondrial DNA polymeraseAleksandra Trifunovic, Anna Wredenberg, Maria Falkenberg, Johannes N. Spelbrink, Anja T. Rovio, Carl E. Bruder, Mohammad Bohlooly-Y, Sebastian Gidlöf, Anders Oldfors, Rolf Wibom, Jan Tornell, Howard T. Jacobs & Nils- Göran Larsson  Presentation by BerilKumcuoglu 04/20/2010
Background Information  mtDNA is in close proximity to the mitochondrial respiratory chain, which causes oxidative damage by the production of reactive oxygen species (ROS). Accumulation of somatic mtDNA mutations were claimed to have a role in aging.  The number of cytochrome c oxidase (COX) deficient cells progressively increases in postmitotic tissues.  ,[object Object]
  Somatic mutations have capacity to cause a variety of aging phenotypes in mammals, but its relative importance in mammalian aging is not clear.  ,[object Object]
Exon 3 ( yellow box) of the targeting vector encodes alanine instead of aspartate.
Restriction with Bg/I shows Frt-flanked PGK-neo casette excision.,[object Object],[object Object]
The median lifespan was 48 weeks.
All of them died before the age of 61 weeks.
Aging Related Phenotypes were first observed at the age of 25 weeks.
 Weight loss
Reduced subcutaneous fat
Alopecia (hair loss)
Kyphosis ( curvature of the spine)

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