Persistence of large mtDNA rearrangements linked to premature aging in Pol γ exonuclease-deficient mice.

Mitochondrial DNA damage patterns directly link to premature aging in mice, unveiling new mechanisms for age-related diseases.

Ultra-sensitive LostArc pipeline sequencing of 10 tissues in POLG exonuclease-deficient mice reveals large mtDNA deletions and rearrangements persist with tissue-specific patterns, mechanistically linking mitochondrial DNA repair fidelity to the premature aging phenotype and establishing new paradigms for mtDNA-driven aging biology.

What the study was

Study design

in_vivo

Category

aging_longevity

Maturity

preclinical

Journal

Nucleic Acids Research

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