Aging drives a program of DNA methylation decay in plant organs [RNA-Seq]
Epigenetic changes are a hallmark of aging in mammals, but their molecular mechanics are poorly understood. 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 and dissect causal relationships. Here, we show that the short-lived model plant species Arabidopsis thaliana exhibits a loss of epigenetic integrity during aging, causing DNA methylation decay in repressive chromatin 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, whilst physical aging remains unaffected. This presents a new paradigm in which a gene regulatory program sets the rate of epigenomic information loss during aging. Overall design: Refer to individual series