A coordinated local translational control point at the synapse involving relief from silencing and MOV10 degradation.

摘要: Persistent changes in synaptic strength are locally regulated by both protein degradation and synthesis; however, the coordination of these opposing limbs is poorly understood. Here, we found that RISC MOV10 was present at synapses rapidly degraded proteasome an NMDA-receptor-mediated activity-dependent manner. We designed a translational trap to capture those mRNAs whose spatiotemporal translation MOV10. When suppressed, set mRNAs--including alpha-CaMKII, Limk1, depalmitoylating enzyme lysophospholipase1 (Lypla1)--selectively entered polysome compartment. also observed Lypla1 mRNA associated with brain-enriched microRNA miR-138. Using photoconvertible reporter, Kaede, analyzed synthesis driven alpha-CaMKII 3'UTRs. established this be dependent. These results suggest unifying picture local regulatory mechanism during plasticity.