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HuD is a neural enhancer of global translation acting on mTORC1-responsive genes and sponged by the Y3 small non-coding RNA

By Paola Zuccotti, Toma Tebaldi, Daniele Peroni, Marcel Köhn, Lisa Gasperini, Valentina Potrich, Tatiana Dudnakova, Guido Sanguinetti, Luciano Conti, Paolo Macchi, David Tollervey, Stefan Hüttelmaier, Alessandro Quattrone

Posted 19 Oct 2017
bioRxiv DOI: 10.1101/205658 (published DOI: 10.1016/j.molcel.2018.06.032)

The RNA-binding protein HuD promotes neurogenesis and favors recovery from peripheral axon injury. HuD interacts with many mRNAs, altering both stability and translation efficiency. UV-crosslinking and analysis of cDNA (CRAC) generated a nucleotide resolution map of the HuD RNA interactome in motor neuron-like cells. HuD target sites were identified in 1304 mRNAs, predominantly in the 3'UTR, with enrichment for genes involved in protein synthesis and axonogenesis. HuD bound many mRNAs encoding mTORC1-responsive ribosomal proteins and translation factors. Altered HuD expression correlated with the translational efficiency of these mRNAs and overall protein synthesis, in a mTORC1-independent fashion. The predominant HuD target was the abundant, small non-coding RNA Y3, which represented 70% of HuD interaction signal. Y3 functions as a molecular sponge for HuD, dynamically limiting its activity. These findings uncover an alternative route to the mTORC1 pathway for translational control in motor neurons that is tunable by a small non-coding RNA.

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