Aging drives a program of DNA methylation decay in plant organs
Abstract
How organisms age is a question with broad implications for human health. In mammals, DNA methylation is a biomarker for biological age, which may predict age more accurately than date of birth. However, limitations in mammalian models make it difficult to identify mechanisms underpinning age-related DNA methylation changes. Here, we show that the short-lived model plant Arabidopsis thaliana exhibits a loss of epigenetic integrity during aging, causing heterochromatin DNA methylation decay and the expression of transposable elements. We show that the rate of epigenetic aging can be manipulated by extending or curtailing lifespan, and that shoot apical meristems are protected from this aging process. We demonstrate that a program of transcriptional repression suppresses DNA methylation maintenance pathways during aging, and that mutants of this mechanism display a complete absence of epigenetic decay. This presents a new paradigm in which a gene regulatory program sets the rate of epigenomic information loss during aging.
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Research summary
The paper investigates the mechanisms of DNA methylation decay during aging in a model plant, which provides insights into the epigenetic aspects of aging. This research is relevant to understanding the biological processes underlying aging, potentially offering insights that could be applicable to longevity research in other organisms, including humans. However, while the findings are important and contribute to the field, they do not represent a major breakthrough or transformative discovery, hence the moderate impact score.
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