Ubiquitin ligase TRIM3 controls hippocampal plasticity and learning by regulating synaptic γ-actin levels

• DOI: 10.1083/jcb.201506048
• Publication Date: 2015-11-03T01:35:27Z
• Authors: Joerg Schreiber; Marlene J. Végh; Julia Dawitz; Tim Kroon; Maarten Loos; Dorthe Labonté; Ka Wan Li; Pim Van Nierop; Michiel T. Van Di...; Chris I. De Zeeuw; Matthias Kneussel; Rhiannon M. Meredith; August B. Smit; Ronald E. Van Kes...
• Keywords: Actin remodeling

Synaptic plasticity requires remodeling of the actin cytoskeleton. Although two isoforms, β- and γ-actin, are expressed in dendritic spines, specific contribution γ-actin expression synaptic is unknown. We show that levels regulated by E3 ubiquitin ligase TRIM3. TRIM3 protein Actg1 transcript colocalized messenger ribonucleoprotein granules responsible for targeting RNAs. polyubiquitylates most likely cotranslationally at sites. Trim3−/− mice consequently have increased hippocampal synapses, resulting higher spine densities, long-term potentiation, enhanced short-term contextual fear memory consolidation. Interestingly, deletion caused an increase memory. Collectively, our findings suggest temporal control required to regulate timing plasticity. propose a model which regulates turnover filament stability thus forms transient inhibitory constraint on