Faculty, Staff and Student Publications

Language

English

Publication Date

12-2-2025

Journal

Nature Communications

DOI

10.1038/s41467-025-65845-2

PMID

41330919

PMCID

PMC12689632

PubMedCentral® Posted Date

12-2-2025

PubMedCentral® Full Text Version

Post-print

Abstract

We analyze 10,986 participants (mean age 77; 63% women; 54% non-White) across seven U.S. cohorts to study the relationship between mitochondrial DNA (mtDNA) heteroplasmy and nuclear DNA methylation. We identify 597 CpGs associated with heteroplasmy burden, generally showing lower methylation. These CpGs are enriched in dynamically regulated island shores and depleted in CpG islands, indicating involvement in context-specific rather than constitutive gene regulation. In HEK293T cells, we introduce a truncating mtDNA mutation (MT-COX3, mt.9979) and observe a positive correlation between variant allele fraction and methylation at cg04569152, supporting a direct mtDNA-nDNA epigenetic link. Many heteroplasmy-associated CpGs overlap with known methylation-trait associations for metabolic and behavioral traits. Composite CpG scores predict all-cause mortality and incident CVD, with one-unit increases associated with 1.27-fold and 1.12-fold higher hazards, respectively. These findings suggest an mtDNA-nDNA epigenetic connection in aging and disease, though its direction and mechanisms remain to be studied.

Keywords

Humans, DNA Methylation, DNA, Mitochondrial, Female, Male, CpG Islands, Aged, Heteroplasmy, Genome-Wide Association Study, Cell Nucleus, HEK293 Cells, Epigenesis, Genetic, Epigenome, Mitochondria, Aged, 80 and over, Middle Aged, Cohort Studies

Published Open-Access

yes

Included in

Public Health Commons

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