BAF53b is a neuron-specific stoichiometric component of BAF complexes not found in other nucleosome remodeling complexes8. To examine the role of BAF53b in long-term memory processes, we engineered transgenic mice that express a mutant form of BAF53b with a deletion of the hydrophobic domain (BAF53bΔHD; see Fig. 1A). The rationale for this deletion is that the hydrophobic domain is predicted to enable protein-protein interactions with other subunits of nBAF complexes, and deletion of this domain in the non-neuronal homolog BAF53a was shown to generate a dominant negative form of BAF53a18. Given the high degree of homology between BAF53a and BAF53b, we predicted a similar dominant-negative impact of deleting the HD from BAF53b. The BAF53bΔHD transgene (Fig. 1A) is expressed by the CaMKIIα promoter19, which allows for restricted expression to forebrain excitatory neurons and postnatal development20. Thus, we avoided developmental effects due to the known role for BAF53b in post mitotic embryonic development. We developed two independent lines of CaMKIIα-BAF53bΔHD. Both lines have normal brain morphology (Supplemental Fig. S1A), but are characterized by significantly different levels of transgene expression in hippocampal
