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Publication : Low-level mitochondrial heteroplasmy modulates DNA replication, glucose metabolism and lifespan in mice.

First Author  Hirose M Year  2018
Journal  Sci Rep Volume  8
Issue  1 Pages  5872
PubMed ID  29651131 Mgi Jnum  J:262576
Mgi Id  MGI:6163098 Doi  10.1038/s41598-018-24290-6
Citation  Hirose M, et al. (2018) Low-level mitochondrial heteroplasmy modulates DNA replication, glucose metabolism and lifespan in mice. Sci Rep 8(1):5872
abstractText  Mutations in mitochondrial DNA (mtDNA) lead to heteroplasmy, i.e., the intracellular coexistence of wild-type and mutant mtDNA strands, which impact a wide spectrum of diseases but also physiological processes, including endurance exercise performance in athletes. However, the phenotypic consequences of limited levels of naturally arising heteroplasmy have not been experimentally studied to date. We hence generated a conplastic mouse strain carrying the mitochondrial genome of an AKR/J mouse strain (B6-mt(AKR)) in a C57BL/6 J nuclear genomic background, leading to >20% heteroplasmy in the origin of light-strand DNA replication (OriL). These conplastic mice demonstrate a shorter lifespan as well as dysregulation of multiple metabolic pathways, culminating in impaired glucose metabolism, compared to that of wild-type C57BL/6 J mice carrying lower levels of heteroplasmy. Our results indicate that physiologically relevant differences in mtDNA heteroplasmy levels at a single, functionally important site impair the metabolic health and lifespan in mice.
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