DRUSE

A paper by Alexandra Kukat and Aleksandra Trifunovic demonstrates that somatic mtDNA mutations have the capacity to cause a variety of aging phenotypes in mammals. However, the relative importance of somatic mtDNA mutations in mammalian aging remains unclear, as the overall mutation load in normal mammalian aging tissues is much lower than needed to cause mitochondrial dysfunction. However, results from single cells argue that despite a relatively low overall level of mtDNA mutations, the mutational load in single cells could be substantial. Therefore, this may result in a functional impairment of the tissue by the loss of critical cells by cellular senescence or cell death.