Université Paris-Saclay, Commissariat à l'Énergie Atomique et aux Énergies Alternatives (CEA), Centre National de la Recherche Scientifique (CNRS), Institute for Integrative Biology of the Cell (I2BC), Gif-sur-Yvette, France.
Institut de Biologie de l'Ecole Normale Supérieure (IBENS), Ecole Normale Supérieure, CNRS, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, Sciences and Lettres (PSL) Research University, Paris, France.
Life Sci Alliance. 2020 Dec 21;4(2). doi: 10.26508/lsa.202000848. Print 2021 Feb.
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.
在植物和哺乳动物中，DNA 甲基化和组蛋白 H3 赖氨酸 27 三甲基化（H3K27me3）分别由多梳抑制复合物 2 沉积，被认为是两种专门的转座元件（TE）和基因的表观遗传沉默系统。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 中表明，在维持 DNA 甲基化缺陷的 突变体中数百个 TE 中观察到的 H3K27me3 的增加，主要取决于卷曲叶（CLF），它是两种在营养组织中具有活性的部分冗余 H3K27 甲基转移酶之一。令人惊讶的是，在 双突变体植物中完全丧失 H3K27me3 并没有伴随着 TE 表达的进一步激活或转座的爆发。相反，与 相比， 植物表现出较少激活的 TE，以及染色质紧凑和连接 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 相关的分子表型，而是部分抑制它们，这对我们关于两种保守的表观遗传沉默途径之间关系的假设提出了挑战。
