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

Area of Science:

• Neuroscience
• Molecular Biology
• Genetics

Background:

• Long-term memory and synaptic plasticity depend on new protein synthesis.
• The precise mechanisms linking learning to this protein synthesis remain largely unknown.
• MicroRNAs regulate gene expression and can silence protein translation at synapses.

Purpose of the Study:

• To investigate the role of Translin/Trax in learning-induced protein synthesis for memory formation.
• To elucidate how Translin/Trax influences microRNA activity at activated synapses.
• To identify downstream targets of Translin/Trax-mediated translational control in memory.

Main Methods:

• Utilized knockout mice lacking Translin/Trax.
• Assessed synaptic tagging and long-term memory performance.
• Analyzed hippocampal microRNA expression and protein levels, specifically targeting ACVR1C.
• Investigated the effects of ACVR1C inhibition.

Main Results:

• Translin/Trax-deficient mice exhibited impaired synaptic tagging and long-term memory.
• Learning induced increased levels of specific microRNAs targeting ACVR1C in these mice.
• The absence of Translin/Trax prevented the learning-induced increase of ACVR1C protein at synapses.
• Inhibition of ACVR1C mimicked the memory deficits observed in Translin/Trax knockout mice.

Conclusions:

• Translin/Trax plays a crucial role in facilitating de novo protein synthesis required for memory.
• Learning triggers Translin/Trax to suppress microRNA-mediated silencing of ACVR1C.
• This pathway, involving Translin/Trax and ACVR1C, represents a novel mechanism for memory formation.