ArticlePloS one2013
Mitochondrial inverted repeats strongly correlate with lifespan: mtDNA inversions and aging.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 51 citations in OpenAlex.
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- High heteroplasmy is associated with low mitochondrial copy number and selection against non-synonymous mutations in the snail Cepaea nemoralis.BMC genomics · 2024Article
- Secondary structure of the human mitochondrial genome affects formation of deletions.BMC biology · 2023Article
- Mitochondrial Genome Evolution of Placozoans: Gene Rearrangements and Repeat Expansions.Genome biology and evolution · 2021Article
- Long-Lived Species of Bivalves Exhibit Low MT-DNA Substitution Rates.Frontiers in molecular biosciences · 2021Article
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- Repetitive DNA profile of the amphibian mitogenome.BMC bioinformatics · 2020Article
- ImtRDB: a database and software for mitochondrial imperfect interspersed repeats annotation.BMC genomics · 2019Article
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- Darwinism for the Genomic Age: Connecting Mutation to Diversification.Frontiers in genetics · 2017Article
- MitoAge: a database for comparative analysis of mitochondrial DNA, with a special focus on animal longevity.Nucleic acids research · 2016Article
- Are mutagenic non D-loop direct repeat motifs in mitochondrial DNA under a negative selection pressure?Nucleic acids research · 2015Article
- Association of G-quadruplex forming sequences with human mtDNA deletion breakpoints.BMC genomics · 2014Article
- The emergence of the mitochondrial genome as a partial regulator of nuclear function is providing new insights into the genetic mechanisms underlying age-related complex disease.Human genetics · 2014Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial defects are implicated in aging and in a multitude of age-related diseases, such as cancer, heart failure, Parkinson's disease, and Huntington's disease. However, it is still unclear how mitochondrial defects arise under normal physiological conditions. Mitochondrial DNA (mtDNA) deletions caused by direct repeats (DRs) are implicated in the formation of mitochondrial defects, however, mitochondrial DRs show relatively weak (Pearson's r = -0.22, p<0.002; Spearman's ρ = -0.12, p = 0.1) correlation with maximum lifespan (MLS). Here we report a stronger correlation (Pearson's r = -0.55, p<10(-16); Spearman's ρ = -0.52, p<10(-14)) between mitochondrial inverted repeats (IRs) and lifespan across 202 species of mammals. We show that, in wild type mice under normal conditions, IRs cause inversions, which arise by replication-dependent mechanism. The inversions accumulate with age in the brain and heart. Our data suggest that IR-mediated inversions are more mutagenic than DR-mediated deletions in mtDNA, and impose stronger constraint on lifespan. Our study identifies IR-induced mitochondrial genome instability during mtDNA replication as a potential cause for mitochondrial defects.
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