DNA deletions and clonal mutations drive premature aging in mitochondrial mutator mice

Mitochondrial DNA (mtDNA) mutations are thought to have a causal role in many age-related pathologies. Here we identify mtDNA deletions as a driving force behind the premature aging phenotype of mitochondrial mutator mice, and provide evidence for a homology-directed DNA repair mechanism in mitochondria that is directly linked to the formation of mtDNA deletions. In addition, our results demonstrate that the rate at which mtDNA mutations reach phenotypic expression differs markedly among tissues, which may be an important factor in determining the tolerance of a tissue to random mitochondrial mutagenesis.     

Differential expression of isozymes in relation to organogenesis in two closely related species

Summary Two closely related species of Gentianaceae were established in tissue culture and transferred to a regeneration medium containing 2,4-D. Even though the age of cultures and all the environmental conditions were identical, only one of them expressed a clear morphogenic potential, and the differences are expressive in the isozyme banding patterns observed for creatine phosphokinase, lactate dehydrogenase and indoleacetaldehyde dehydrogenase. No differences in alkaline phosphatase isozymes were detected.This work was supported in part by the National Science Foundation (No. DCB 8 611 889) USA with a grant to the senior author.