背景回顾：DNA methylation has evolved to silence mutagenic transposable elements (TEs) while typically avoiding the targeting of endogenous genes. Mechanisms that prevent DNA methyltransferases from ectopically methylating genes are expected to be of prime importance during periods of dynamic cell cycle activities including plant embryogenesis. 

提出问题：However, virtually nothing is known regarding how DNA methyltransferase activities are precisely regulated during embryogenesis to prevent the induction of potentially deleterious and mitotically stable genic epimutations. 

结果1：Here, we report that microRNA-mediated repression of CHROMOMETHYLASE 3 (CMT3) and the chromatin features that CMT3 prefers help prevent ectopic methylation of thousands of genes during embryogenesis that can persist for weeks afterwards. 

结果2：Our results are also consistent with CMT3-induced ectopic methylation of promoters or bodies of genes undergoing transcriptional activation reducing their expression. 

结论：Therefore, the repression of CMT3 prevents epigenetic collateral damage on endogenous genes. We also provide a model that may help reconcile conflicting viewpoints regarding the functions of gene-body methylation that occurs in nearly all flowering plants.

 摘 要 

DNA甲基化演化为沉默诱变性转座因子（TEs）的机制，同时又能够避免对内源性基因的靶向。在包括植物胚胎发生在内的动态细胞周期活动过程中，防止DNA甲基转移酶异位甲基化基因的机制，对于生物来说是极其重要的。然而，关于DNA甲基转移酶活性在胚胎发生过程中如何被精确调控，以防止潜在有害的、有丝分裂稳定的遗传表观突变诱导方面的机制所知甚少。本文中，作者报道了植物胚胎发生过程中，microRNA介导的CMT3抑制以及CMT3偏好的染色质特征，有助于防止数千个基因的异位甲基化，这种状态可能会持续数周。本文的结果与CMT3诱导的正在经历转录激活的基因的启动子或基因区异位甲基化，导致其表达量下降的结果一致。因此，抑制CMT3可以防止内源性基因的表观遗传附带损伤。作者在本文中还提供了一个模型，可以帮助解释几乎所有开花植物中都会发生的基因区甲基化功能的争议观点。