Mitochondria and aging do duplicated mtDNA control regions confer longer lifespans in parrots


Meeting Abstract

39.5  Wednesday, Jan. 5  Mitochondria and aging: do duplicated mtDNA control regions confer longer lifespans in parrots? WRIGHT, T.F.*; SCHIRTZINGER, E.E.; YOUNG, A.M.; HOBSON, E.A.; EBERHARD, J.R.; New Mexico State University; New Mexico State University; New Mexico State University; New Mexico State University; Louisiana State University wright@nmsu.edu

The mitochondrial theory of aging suggests that reactive oxygen species produced in the mitochondria during respiration damage the mitochondrial genome, thereby accelerating cellular senescence and shortening organismal lifespan. Although size and gene order are generally conserved in mitochondrial genomes, duplications of the mtDNA control region (CR) have been observed in a range of taxa. In most cases, duplicated CR degrade over time, but in some, including the long-lived albatrosses and parrots, duplicated CRs are maintained in an apparently functional state. These observations have led to the hypothesis that duplicated CRs confer longer lifespan. We tested this hypothesis in parrots (Psittaciformes) by 1) surveying 117 parrot species for presence of duplicated control regions, 2) collecting lifespan data on 262 species from 87,777 records in the ISIS zoo database, and 3) constructing a molecular phylogeny of the parrots using 5 gene regions. 38 species showed evidence of a duplicated CR; reconstructions on the phylogeny revealed 6 independent origins of duplications and no losses. Maximum lifespan varied widely among species: the highest was 92 years in Cacatua moluccensis, but only 11 other species had lifespans over 50 years. Body mass was a significant predictor of lifespan with larger species living longer. There was no relationship between the presence of a duplicated CR and lifespan corrected for body mass either when species were treated as independent points or with phylogenetically-corrected independent contrasts. These results do not support the hypothesis that mtDNA CR duplications are maintained through a positive effect on organismal lifespan.

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