MEF2C and HDAC5 regulate Egr1 and Arc genes to increase dendritic spine density and complexity in early enriched environment.

Q4 Neuroscience

Neuronal signaling Pub Date : 2020-07-23 eCollection Date: 2020-09-01 DOI:10.1042/NS20190147

Shu Juan Puang, Bavani Elanggovan, Tendy Ching, Judy C G Sng

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引用次数: 3

Abstract

We investigated the effects of environmental enrichment during critical period of early postnatal life and how it interplays with the epigenome to affect experience-dependent visual cortical plasticity. Mice raised in an EE from birth to during CP have increased spine density and dendritic complexity in the visual cortex. EE upregulates synaptic plasticity genes, Arc and Egr1, and a transcription factor MEF2C. We also observed an increase in MEF2C binding to the promoters of Arc and Egr1. In addition, pups raised in EE show a reduction in HDAC5 and its binding to promoters of Mef2c, Arc and Egr1 genes. With an overexpression of Mef2c, neurite outgrowth increased in complexity. Our results suggest a possible underlying molecular mechanism of EE, acting through MEF2C and HDAC5, which drive Arc and Egr1. This could lead to the observed increased dendritic spine density and complexity induced by early EE.

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MEF2C和HDAC5调控Egr1和Arc基因，在早期富集环境中增加树突棘密度和复杂性。

我们研究了在出生后早期生命的关键时期环境富集的影响，以及它如何与表观基因组相互作用，影响经验依赖的视觉皮层可塑性。从出生到CP期间在EE环境中长大的小鼠脊柱密度和视觉皮层树突复杂性增加。EE上调突触可塑性基因Arc和Egr1以及转录因子MEF2C。我们还观察到MEF2C与Arc和Egr1启动子结合的增加。此外，在EE环境中饲养的幼崽HDAC5及其与Mef2c、Arc和Egr1基因启动子的结合减少。随着Mef2c的过表达，神经突生长的复杂性增加。我们的研究结果表明，EE的潜在分子机制可能通过MEF2C和HDAC5驱动Arc和Egr1。这可能导致早期EE引起的树突棘密度和复杂性的增加。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neuronal signaling

CiteScore

4.60

自引率

0.00%

发文量

审稿时长

14 weeks