Abstract
In many plant species, a subset of transcribed genes are characterized by strictly CG-context DNA methylation, referred to as gene body methylation (gbM). The mechanisms that establish gbM are unclear, yet flowering plant species naturally without gbM lack the DNA methyltransferase, CMT3, which maintains CHG (H = A, C, or T) and not CG methylation at constitutive heterochromatin. Here, we identify the mechanistic basis for gbM establishment by expressing CMT3 in a species naturally lacking CMT3. CMT3 expression reconstituted gbM through a progression of de novo CHG methylation on expressed genes, followed by the accumulation of CG methylation that could be inherited even following loss of the CMT3 transgene. Thus, gbM likely originates from the simultaneous targeting of loci by pathways that promote euchromatin and heterochromatin, which primes genes for the formation of stably inherited epimutations in the form of CG DNA methylation.
Highlights
Heritable gains or losses of DNA methylation, or epimutations, can have important phenotypic consequences
Whole genome bisulfite sequencing was completed on individual plants for each generation of each line to assess the impact of A. thaliana CMT3 (AtCMT3) expression on DNA methylation
We have provided experimental evidence that CHROMOMETHYLASE 3 (CMT3) can initiate epimutations in the form of gene body CG methylation, which are maintained over generational time, even after loss of AtCMT3 expression
Summary
Heritable gains or losses of DNA methylation, or epimutations, can have important phenotypic consequences. One form of genic DNA methylation that may provide clues to the mechanisms of epimutation is gene body methylation (gbM), which is found on a subset of expressed genes in many eukaryotic genomes, including most flowering plants (Bewick et al, 2017; Bewick and Schmitz, 2017; Cokus et al, 2008; Feng et al, 2010; Huff and Zilberman, 2014; Lister et al, 2008; Niederhuth et al, 2016; Regulski et al, 2013; Seymour et al, 2014; Takuno and Gaut, 2013; Takuno et al, 2016; Tran et al, 2005; Wang et al, 2015; Zemach et al, 2010; Zhang et al, 2006; Zilberman et al, 2007). The results provide new insights to the mechanism of CMT3-initiation of gbM by demonstrating that CMT3 promotes the establishment of genic CG epimutations which can be maintained even in the absence of CMT3
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