In addition to the BAF53bΔHD mice, we also examined BAF53b heterozygous null animals (Baf53b+/−)8. Baf53b−/− homozygous knockout mice have a complete loss of BAF53b mRNA and protein, and die within the first two postnatal days8. Consistent with the exclusive expression of BAF53b in post mitotic neurons, they have no detectable defects outside of the nervous system8. In contrast, Baf53b+/− het mice develop normally (Supplemental Fig. S1) and express approximately 50% of the wildtype levels of Baf53b mRNA (Fig. 1D) and protein (Fig. 1E). Baf53b mRNA and protein expression in Baf53b+/− het mice was half of that in wildtype littermates both from homecage samples and after training (sacrificed 30min post OLM training; see Fig 2A for schematic diagram) (Fig 1D & 1E). Importantly, there are no neuron-specific homologs of BAF53b that could compensate for its decreased expression. Thus, these results demonstrate that there is no compensation in expression in the Baf53b+/− het mice following behavior. In addition, both anxiety and motor function were found to be normal in BAF53bΔHD and Baf53b+/− het mice as compared to wildtype controls (Supplemental Fig. S2), allowing us to examine memory processes in these mice.
