In plants and mammals, DNA methylation and histone H3 lysine 27 trimethylation (H3K27me3), which is deposited by the polycomb repressive complex 2, are considered as two specialized systems for the epigenetic silencing of transposable element (TE) and genes, respectively. Nevertheless, many TE sequences acquire H3K27me3 when DNA methylation is lost. Here, we show in that the gain of H3K27me3 observed at hundreds of TEs in the mutant defective in the maintenance of DNA methylation, essentially depends on CURLY LEAF (CLF), one of two partially redundant H3K27 methyltransferases active in vegetative tissues. Surprisingly, the complete loss of H3K27me3 in double mutant plants was not associated with further reactivation of TE expression nor with a burst of transposition. Instead, plants exhibited less activated TEs, and a chromatin recompaction as well as hypermethylation of linker DNA compared with Thus, a mutation in polycomb repressive complex 2 does not aggravate the molecular phenotypes linked to but instead partially suppresses them, challenging our assumptions of the relationship between two conserved epigenetic silencing pathways.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7756957 | PMC |
http://dx.doi.org/10.26508/lsa.202000848 | DOI Listing |
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