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 Arabidopsis thaliana that the gain of H3K27me3 observed at hundreds of TEs in the ddm1 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 ddm1 clf double mutant plants was not associated with further reactivation of TE expression nor with a burst of transposition. Instead, ddm1 clf plants exhibited less activated TEs, and a chromatin recompaction as well as hypermethylation of linker DNA compared with ddm1 Thus, a mutation in polycomb repressive complex 2 does not aggravate the molecular phenotypes linked to ddm1 but instead partially suppresses them, challenging our assumptions of the relationship between two conserved epigenetic silencing pathways.

中文翻译：

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Polycomb 突变体部分抑制拟南芥中 DNA 低甲基化相关表型。

在植物和哺乳动物中，由多梳抑制复合物 2 沉积的 DNA 甲基化和组蛋白 H3 赖氨酸 27 三甲基化 (H3K27me3) 被认为是分别用于转座元件 (TE) 和基因表观遗传沉默的两个专门系统。然而，当 DNA 甲基化丢失时，许多 TE 序列会获得 H3K27me3。在这里，我们在拟南芥中表明，在维持 DNA 甲基化有缺陷的ddm1突变体中，在数百个 TE 处观察到的 H3K27me3 增益基本上取决于卷叶（CLF），它是在营养组织中活跃的两种部分冗余的 H3K27 甲基转移酶之一。令人惊讶的是，ddm1 clf中 H3K27me3 的完全丢失双突变植物与 TE 表达的进一步重新激活无关，也与转座爆发无关。相反，与ddm1 相比，ddm1 clf植物表现出较少的活化 TE，染色质再压实以及接头 DNA 的超甲基化因此，多梳抑制复合物 2 中的突变不会加重与ddm1相关的分子表型，而是部分抑制它们，挑战我们两个保守的表观遗传沉默途径之间关系的假设。