Longevity and the evolution of the mitochondrial DNA-coded proteins in mammals.
The amino acids sequences of the mitochondrial DNA-coded peptides of placental mammals evolved at different rates in different branches of the mammalian phylogenetic tree. Adaptive selection was suggested to account for the faster evolution of some mitochondrial DNA-coded proteins in several branches of the mammalian tree, but the driving force(s) for the accelerated evolution has not been elucidated. Mitochondria generate reactive oxygen species (ROS) that appear to constrain the life span of many species. Therefore, I tested the hypothesis that the evolution of mammalian longevity drives the accelerated evolution of mitochondrial DNA-coded peptides. Using rodents as an outgroup for a clad that included most placental mammals (excluding rodents and hedgehogs) the computed rates of amino acid substitution per site were positively correlated with genus longevity (maximal observed averaged life span) for most of the mitochondrial DNA-coded peptides. The substitution per site of ATP6, the proton conducting subunit of ATPsynthase, CYTB, the core subunit of ubiquinone oxidoreductase that participate in both electron and proton transport, and ND3, a subunit of NADH dehydrogenase, showed the strongest correlations with longevity. Additional confirmation for the hypothesis was obtained by the observation that the genetic distances between placental mammals species that belong to different orders are positively correlated with the sum of longevities of the species pairs. The substitutions per site for the entire amino acid sequence coded by the heavy strand mtDNA were also positively correlated with the average longevities of the placental mammals orders. These results support the hypothesis that the evolution of longevity in mammals drove the accelerated evolution of mtDNA-coded peptide. It is suggested that, in mammals, adaptive selection of mutations that decrease the rate of production of reactive oxygen species, directly or indirectly (e.g. by increasing proton leak), increases longevity.
Rottenberg
Hagai
H
New Hope Biomedical R&D, 23 W. Bridge Street, New Hope, PA 18938, USA. rotteh@hotmail.com
D000818:Animals; D004272:DNA, Mitochondrial / Q000737:chemistry / Q000235:genetics*; D030541:Databases, Genetic; D019143:Evolution, Molecular; D016014:Linear Models; D008136:Longevity / Q000235:genetics*; D008322:Mammals / Q000235:genetics* / Q000502:physiology; D008928:Mitochondria / Q000235:genetics / Q000502:physiology; D024101:Mitochondrial Proteins / Q000235:genetics* / Q000502:physiology; D010802:Phylogeny; D017382:Reactive Oxygen Species; D016415:Sequence Alignment
D004272:DNA, Mitochondrial; D024101:Mitochondrial Proteins; D017382:Reactive Oxygen Species