In summary, recent studies have shown that mutations in various subunits of the BAF complex cause intellectual disability disorders in humans12-17 and elegant studies in culture have demonstrated that BAF53b in particular is necessary for dendritic outgrowth8. However, there remained no clear evidence linking BAF-mediated nucleosome remodeling to cognition. In this study, we demonstrate for the first time that the neuron-specific BAF53b subunit of the neuronal BAF complex is necessary for synaptic plasticity and long-term memory processes, likely via the regulation of gene expression required for spine structure and function. These findings support the overall idea that impaired nucleosome remodeling may be a key underlying mechanism to intellectual disability disorders.
