The RNA Seq data indicates that spine abnormalities may be due to altered BAF53b-mediated gene expression. In the Baf53b+/− het mice several key postsynaptic density genes involved in spine plasticity showed altered expression, including multiple regulators of the Rac-PAK and RhoA-LIMK pathways. For example, mir132 expression was increased following OLM training in wildtype mice, but not in Baf53b+/− het mice. Mir132 has previously been shown to regulate spine plasticity39,40 and long-term OLM41 by regulating Rac1 activity through translational repression of p250GAP39. Mir132 also blocks the translation of methyl CpG-binding protein 2 (MeCP2)44, a transcriptional repressor that interacts with methylated DNA. MeCP2 mutant mice have impairments in a synaptic plasticity and a variety of behaviors including long-term memory formation (for review see 45) indicating a critical role for MeCP2 in normal brain function. In humans mutations in MeCP2 have been linked to Rett syndrome, a developmental disorder characterized by cognitive deficits similar to autism46. In addition to mir132, Baf53b+/− het mice have alterations in gene expression of other key regulators of the Rac-PAK and RhoA-LIMK pathways, both at the level of
