Abstract
Rubinstein–Taybi Syndrome (RTS), where the transcriptional co-activator and histone acetyltransferase CBP is mutated and haploinsufficient, is often associated with epilepsy, a disorder that is frequently due to perturbations in the generation of GABAergic interneurons and/or the inhibitory neurotransmitter GABA. Hereby, Tsui et al., recently published in Developmental Biology, asked whether CBP was necessary for the appropriate genesis and differentiation of interneurons in the murine forebrain. This paper defined multiple roles of CBP during forebrain interneuron development. In particular, CBP not only acts as a pro-differentiation factor to enhance the differentiation of ventral forebrain precursors to interneurons, but also modulates the maturation of interneurons by promoting acquisition of a GABAergic interneuron phenotype in the newborn neurons. Thus, deficits in interneuron development caused by CBP haploinsufficiency provide a potential explanation for the epilepsy seen in individuals with RTS.
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