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, Ted Abel*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

12 Citations (Scopus)
276 Downloads (Pure)

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.

Original languageEnglish
Article numbere27872
Number of pages19
JournaleLife
Volume6
DOIs
Publication statusPublished - 20-Sep-2017

Keywords

  • LONG-TERM POTENTIATION
  • BINDING PROTEIN
  • MESSENGER-RNA
  • TESTIS-BRAIN
  • SYNAPTIC PLASTICITY
  • CAPTURE HYPOTHESIS
  • DEPENDENT MEMORY
  • GENE-EXPRESSION
  • RISC ACTIVATION
  • MICE

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