Rapid reversal of translational silencing: Emerging role of microRNA degradation pathways in neuronal plasticity.
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.
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.
Xiuping
X
Fu
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.
Aparna
A
Shah
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. Electronic address: jay.baraban@gmail.com.
Jay M
JM
Baraban
D000818:Animals; D006801:Humans; D035683:MicroRNAs / Q000378:metabolism*; D009473:Neuronal Plasticity / Q000502:physiology*; D014176:Protein Biosynthesis / Q000502:physiology*; D016601:RNA-Binding Proteins / Q000378:metabolism*
D035683:MicroRNAs; D016601:RNA-Binding Proteins
Lin-28; MicroRNA; Plasticity; Pre-microRNA degradation; Silencing; Translin; Trax