Fu Xiuping, Shah Aparna, Baraban Jay M
Solomon H. Snyder Department of Neuroscience and Department of Psychiatry and Behavioral Sciences, Johns Hopkins School of Medicine, 725 N. Wolfe Street, Baltimore, MD 21205, United States.
Solomon H. Snyder Department of Neuroscience and Department of Psychiatry and Behavioral Sciences, Johns Hopkins School of Medicine, 725 N. Wolfe Street, Baltimore, MD 21205, United States.
Neurobiol Learn Mem. 2016 Sep;133:225-232. doi: 10.1016/j.nlm.2016.04.006. Epub 2016 Apr 20.
As microRNAs silence translation, rapid reversal of this process has emerged as an attractive mechanism for driving de novo protein synthesis mediating neuronal plasticity. Herein, we summarize recent studies identifying neuronal stimuli that trigger rapid decreases in microRNA levels and reverse translational silencing of plasticity transcripts. Although these findings indicate that neuronal stimulation elicits rapid degradation of selected microRNAs, we are only beginning to decipher the molecular pathways involved. Accordingly, we present an overview of several molecular pathways implicated in mediating microRNA degradation: Lin-28, translin/trax, and MCPIP1. As these degradation pathways target distinct subsets of microRNAs, they enable neurons to reverse silencing rapidly, yet selectively.
由于微小RNA会使翻译沉默,快速逆转这一过程已成为驱动从头蛋白质合成以介导神经元可塑性的一种有吸引力的机制。在此,我们总结了最近的研究,这些研究确定了触发微小RNA水平快速下降并逆转可塑性转录本翻译沉默的神经元刺激因素。尽管这些发现表明神经元刺激会引发特定微小RNA的快速降解,但我们才刚刚开始破解其中涉及的分子途径。因此,我们概述了几种与介导微小RNA降解有关的分子途径:Lin-28、转铁蛋白/转铁蛋白X(translin/trax)和MCPIP1。由于这些降解途径针对不同的微小RNA亚群,它们使神经元能够快速但有选择地逆转沉默。