Neuronal Elav-like (Hu) proteins regulate RNA splicing and abundance to control glutamate levels and neuronal excitability.

Publication Type Academic Article
Authors Ince-Dunn G, Okano H, Jensen K, Park W, Zhong R, Ule J, Mele A, Fak J, Yang C, Zhang C, Yoo J, Herre M, Okano H, Noebels J, Darnell R
Journal Neuron
Volume 75
Issue 6
Pagination 1067-80
Date Published 09/20/2012
ISSN 1097-4199
Keywords Brain, ELAV Proteins, Gene Expression Regulation, Glutamic Acid, Neurons, RNA Splicing
Abstract The paraneoplastic neurologic disorders target several families of neuron-specific RNA binding proteins (RNABPs), revealing that there are unique aspects of gene expression regulation in the mammalian brain. Here, we used HITS-CLIP to determine robust binding sites targeted by the neuronal Elav-like (nElavl) RNABPs. Surprisingly, nElav protein binds preferentially to GU-rich sequences in vivo and in vitro, with secondary binding to AU-rich sequences. nElavl null mice were used to validate the consequence of these binding events in the brain, demonstrating that they bind intronic sequences in a position dependent manner to regulate alternative splicing and to 3'UTR sequences to regulate mRNA levels. These controls converge on the glutamate synthesis pathway in neurons; nElavl proteins are required to maintain neurotransmitter glutamate levels, and the lack of nElavl leads to spontaneous epileptic seizure activity. The genome-wide analysis of nElavl targets reveals that one function of neuron-specific RNABPs is to control excitation-inhibition balance in the brain.
DOI 10.1016/j.neuron.2012.07.009
PubMed ID 22998874
PubMed Central ID PMC3517991
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