Abstract
Epigenetic states are stably propagated in eukaryotes. In plants, DNA methylation patterns are faithfully inherited over many generations but it is unknown how the dynamic activities of cytosine DNA methyltransferases and 5-methylcytosine DNA glycosylases interact to maintain epigenetic homeostasis. Here we show that a methylation-sensing gene regulatory circuit centered on a 5-methylcytosine DNA glycosylase gene is required for long-term epigenetic fidelity in Arabidopsis. Disrupting this circuit causes widespread methylation losses and abnormal phenotypes that progressively worsen over generations. In heterochromatin, these losses are counteracted such that methylation returns to a normal level over four generations. However, thousands of loci in euchromatin progressively lose DNA methylation between generations and remain unmethylated. We conclude that an actively maintained equilibrium between methylation and demethylation activities is required to ensure long-term stable inheritance of epigenetic information.
Highlights
The MIT Faculty has made this article openly available
We recently discovered that the expression of the Arabidopsis 5-methylcytosine DNA glycosylase gene ROS1 is activated by the RNA-directed DNA methylation pathway (RdDM) pathway and repressed by DNA demethylation by the ROS1 enzyme[13]
No abnormal phenotypes were apparent in BRmut control lines, indicating that the curled leaf phenotype is dependent on ROS1 (Fig. 1c)
Summary
The MIT Faculty has made this article openly available. Please share how this access benefits you. We show that a methylation-sensing gene regulatory circuit centered on a 5-methylcytosine DNA glycosylase gene is required for long-term epigenetic fidelity in Arabidopsis Disrupting this circuit causes widespread methylation losses and abnormal phenotypes that progressively worsen over generations. We recently discovered that the expression of the Arabidopsis 5-methylcytosine DNA glycosylase gene ROS1 is activated by the RdDM pathway and repressed by DNA demethylation by the ROS1 enzyme[13] These pathways converge at a short 220 bp sequence in the ROS1 5′ region[13,14], such that ROS1 transcriptional output is quantitatively coupled to the methylation level of this sequence. Restoring ROS1 expression to wild-type levels in a methylation mutant causes abnormal phenotypes that worsen over multiple generations This causes widespread methylation losses across the genome. We conclude that the regulation of ROS1 by methylation and demethylation pathways functions as a methylation-sensing circuit that buffers against fluctuations or instability in the maintenance of DNA methylation patterns over long periods of time
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