Mitochondrial DNA progressively accumulates N6-methyladenine (6mA) with age, potentially serving as an ageing biomarker. In long-lived mutants, this methylation rate slows, linking mitochondrial epigenetics to longevity. The findings highlight mitochondrial DNA’s role in ageing and introduce a precise, cost-effective method for measuring 6mA levels.
October 2023 – International Journal of Molecular Sciences
Key takeaways
- N6-Methyladenine (6mA) accumulates with age in mitochondrial DNA, linking epigenetic changes to ageing: Over time, the levels of 6mA in mitochondrial DNA progressively increase, suggesting a direct relationship between mitochondrial epigenetic modifications and the ageing process. This accumulation may contribute to mitochondrial dysfunction, a hallmark of ageing, and highlights the importance of mitochondrial health in promoting longevity
- Slower 6mA accumulation in long-lived organisms reveals a link between methylation dynamics and lifespan: In long-lived mutant organisms, such as those with reduced insulin-like growth factor signalling, the rate of 6mA accumulation in mitochondrial DNA is significantly slower. This highlights the potential for interventions that influence methylation processes to extend lifespan and improve healthspan
- 6mA levels in mitochondrial DNA could serve as a reliable biomarker of biological age: The consistent correlation between 6mA levels and age provides a promising tool for assessing biological age. This biomarker offers a cost-effective and accurate method for estimating age, which could be valuable in personalised medicine and longevity research
Enzymes responsible for adding and removing 6mA in mitochondrial DNA are pivotal in regulating its levels. By modulating the activity of these enzymes, it may be possible to influence mitochondrial function and slow the ageing process, presenting new opportunities for therapies aimed at extending lifespan and improving overall health.
Read the article at: Sturm, Ádám, et al. “N6-Methyladenine Progressively Accumulates in Mitochondrial DNA During Aging.” International Journal of Molecular Sciences, vol. 24, no. 19, 2023, Article 14858, doi:10.3390/ijms241914858.