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首页> 外文期刊>Neurobiology of learning and memory >Dynamic association of epigenetic H3K4me3 and DNA 5hmC marks in the dorsal hippocampus and anterior cingulate cortex following reactivation of a fear memory
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Dynamic association of epigenetic H3K4me3 and DNA 5hmC marks in the dorsal hippocampus and anterior cingulate cortex following reactivation of a fear memory

机译：表观遗传H3K4ME3和DNA 5HMC标记的动态关联在背部海马和前铰接后的再激活后恐惧记忆

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Epigenetic mechanisms such as DNA methylation and histone methylation are critical regulators of gene transcription changes during memory consolidation. However, it is unknown how these epigenetic modifications coordinate control of gene expression following reactivation of a previously consolidated memory. Here, we found that retrieval of a recent contextual fear conditioned memory increased global levels of H3 lysine 4-trimethylation (H3K4me3) and DNA 5-hydroxymethylation (5hmC) in area CA1 of the dorsal hippocampus. Further experiments revealed increased levels of H3K4me3 and DNA 5hmC within a CpG-enriched coding region of the Npas4, but not c-fos, gene. Intriguingly, retrieval of a 30-day old memory increased H3K4me3 and DNA 5hmC levels at a CpG-enriched coding region of c-fos, but not Npas4, in the anterior cingulate cortex, suggesting that while these two epigenetic mechanisms co-occur following the retrieval of a recent or remote memory, their gene targets differ depending on the brain region. Additionally, we found that in vivo siRNA-mediated knockdown of the H3K4me3 methyltransferase MIII in CA1 abolished retrieval-induced increases in DNA 5hmC levels at the Npas4 gene, suggesting that H3K4me3 couples to DNA 5hmC mechanisms. Consistent with this, loss of MITI prevented retrieval induced increases in Npas4 mRNA levels in CA1 and impaired fear memory. Collectively, these findings suggest an important link between histone methylation and DNA hydroxymethylation mechanisms in the epigenetic control of de novo gene transcription triggered by memory retrieval. (C) 2017 Elsevier Inc. All rights reserved.
机译：表观遗传机制，如DNA甲基化和组蛋白甲基化是在记忆合并期间基因转录变化的临界调节因子。然而，尚不清楚这些表观遗传修饰如何在重新激活先前固结的记忆后对基因表达的控制。在这里，我们发现检索最近的上下文恐惧条件内存增加了背部海马的区域Ca1中的H3赖氨酸4-三甲基化（H3K4ME3）和DNA 5-羟甲基（5HMC）的全球水平。进一步的实验揭示了NPAS4的CPG富集的编码区内的H3K4ME3和DNA 5HMC水平增加，但不是C-FOS，基因。有趣的是，30天旧记忆的检索增加了H3K4ME3和DNA 5HMC水平，在富集的C-FOS的CPG富集的编码区，而不是NPAS4，表明这两种表观遗传机制在后面发生了共同发生检索最近或远程记忆，它们的基因目标根据大脑区域而异。另外，我们发现，在CA1中的H3K4ME3甲基转移酶MIII的体内siRNA介导的敲除废除了NPAS4基因的DNA 5HMC水平的检索诱导的增加，表明H3K4ME3与DNA 5HMC机制致作用。符合这一致的是，MITI的丧失阻止检索诱导的CA1中NPAS4 mRNA水平的增加和恐惧记忆受损。总的来说，这些研究结果表明，通过记忆检索触发的德诺人基因转录的表观遗传控制中的组蛋白甲基化和DNA羟甲基化机制的重要联系。 （c）2017年Elsevier Inc.保留所有权利。

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