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Learning induces the translin/trax RNase complex to express activin receptors for persistent memory
Journal article   Open access   Peer reviewed

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

Alan Jung Park, Robbert Havekes, Xiuping Fu, Rolf Hansen, Jennifer C Tudor, Lucia Peixoto, Zhi Li, Yen-Ching Wu, Shane G Poplawski, Jay M Baraban, …
eLife, Vol.6, e27872
09/20/2017
DOI: 10.7554/eLife.27872
PMCID: PMC5606845
PMID: 28927503
url
https://doi.org/10.7554/eLife.27872View
Published (Version of record) Open Access

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-β 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.
Gene Expression DNA-Binding Proteins - metabolism Learning Animals Neuronal Plasticity Memory Activin Receptors, Type I - metabolism Mice Hippocampus - physiology RNA-Binding Proteins - metabolism Ribonucleases - metabolism

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