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Learning induces the translin/trax RNase complex to express activin receptors for persistent memory

Cited 22 time in Web of Science Cited 26 time in Scopus
Authors

Park, Alan Jung; Havekes, Robbert; Fu, Xiuping; Hansen, Rolf; Tudor, Jennifer C.; Peixoto, Lucia; Li, Zhi; Wu, Yen-Ching; Poplawski, Shane G.; Baraban, Jay M.; Abel, Ted

Issue Date
2017-09
Publisher
ELIFE SCIENCES PUBLICATIONS LTD
Citation
ELIFE, Vol.6
Abstract
Long-lasting forms of synaptic plasticity and memory require de novo protein synthesis. Yet, how learning triggers this process to form memory is unclear. Translin/trax is a candidate to drive this learning-induced memory mechanism by suppressing microRNA-mediated translational silencing at activated synapses. We find that mice lacking translin/trax display defects in synaptic tagging, which requires protein synthesis at activated synapses, and long-term memory. Hippocampal samples harvested from these mice following learning show increases in several disease-related microRNAs targeting the activin A receptor type 1C (ACVR1C), a component of the transforming growth factor-beta receptor superfamily. Furthermore, the absence of translin/trax abolishes synaptic upregulation of ACVR1C protein after learning. Finally, synaptic tagging and long-term memory deficits in mice lacking translin/trax are mimicked by ACVR1C inhibition. Thus, we define a new memory mechanism by which learning reverses microRNA-mediated silencing of the novel plasticity protein ACVR1C via translin/trax.
ISSN
2050-084X
URI
https://hdl.handle.net/10371/203377
DOI
https://doi.org/10.7554/eLife.27872
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  • College of Medicine
Research Area Computational decoding, Electrophysiology, Neuroscience

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