News Release

Ribosomal DNA methylation patterns reveal when aging begins

“Our results suggest that rDNA promoter methylation and the age-related loss of active rDNA TU, which are a hallmark of the aging process, start only after reaching sexual maturity.”

Peer-Reviewed Publication

Impact Journals LLC

rDNA copy number variation and methylation from birth to sexual maturity

image: 

Figure 1. UCE/CP methylation, absolute, and active CN in young individuals. (A) Mean methylation (Y axis) of the UCE/CP does not increase with age (X axis). Red dots represent blood samples of 139 healthy controls and blue dots of 141 individuals with DD. (B) UCE/CP methylation (Y axis) is significantly positively correlated with absolute rDNA CN (X axis). (CD) Both the absolute number of rDNA TU (C) and active CN (D) remain stable during the first 20 years of life. There are no significant between-group differences.

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Credit: Copyright: © 2025 Michler et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

“Our results suggest that rDNA promoter methylation and the age-related loss of active rDNA TU, which are a hallmark of the aging process, start only after reaching sexual maturity.”

BUFFALO, NY — July 23, 2025 — A new research paper was published in Aging (Aging-US) Volume 17, Issue 6, on June 16, 2025, titled “rDNA copy number variation and methylation from birth to sexual maturity.”

In this study, led by first authors Alina Michler and Sarah Kießling along with corresponding author Thomas Haaf from Julius Maximilians University in Germany, researchers explored how ribosomal DNA (rDNA) copy number and methylation change from infancy to adolescence. They discovered that the epigenetic changes often associated with aging in adults do not occur before sexual maturity. This finding offers new insights into when the biological aging process truly begins.

Ribosomal DNA plays a critical role in producing proteins essential for cell survival. The researchers analyzed blood samples from 280 individuals, ranging from newborns to 18 years of age, including healthy individuals and those with developmental delays. They measured the number of rDNA copies and examined how genes are switched on or off through methylation, a chemical modification of DNA. The results showed that while adults experience a gradual loss of active rDNA copies and increased methylation—a hallmark of aging—these changes were absent in children and teenagers. In fact, during childhood and adolescence, the number of active, unmethylated rDNA copies slightly increased.

These findings support the long-debated idea that biological aging begins only after the body reaches reproductive maturity. Until that point, cells appear to actively maintain rDNA in a youthful state, ensuring that protein production remains efficient. This may help explain why children and teenagers are better at resisting many age-related diseases and why their cells recover more easily from stress.

The study also shows that changes in rDNA copy numbers are not associated with unexplained developmental delays. This suggests these epigenetic processes are probably not involved in early-life syndromes. The findings highlight how the body works to preserve genetic stability during childhood and raise important questions about what triggers the shift to aging-related changes after puberty.

“Collectively our data suggest that the rDNA hypomethylation state is actively maintained in somatic tissues of young individuals.”

The insights gained from this research expand the understanding of the molecular clock of aging. They suggest potential new ways to delay aging processes by exploring how youthful rDNA methylation patterns are maintained. As scientists continue to investigate these mechanisms, the study provides a clear foundation for future research aimed at extending cellular health beyond adolescence.

Read the full paper: DOIhttps://doi.org/10.18632/aging.206271

Corresponding author: Thomas Haaf – thomas.haaf@uni-wuerzburg.de

Keywords: aging, absolute rDNA copy number, active rDNA copy number, deep bisulfite sequencing, developmental delay, droplet digital PCR

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