| First Author | Park AJ | Year | 2017 |
| Journal | Elife | Volume | 6 |
| PubMed ID | 28927503 | Mgi Jnum | J:247310 |
| Mgi Id | MGI:5915178 | Doi | 10.7554/eLife.27872 |
| Citation | Park AJ, et al. (2017) Learning induces the translin/trax RNase complex to express activin receptors for persistent memory. Elife 6:e27872 |
| abstractText | 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. |
