We observed important transition states by analyzing single-cell data. Specifically, we found that SST+ interneurons were present at various levels of maturity at D54. SST cell death has been observed in mood disorders and dysfunctional SST interneurons have recently been shown to exacerbate cortical excitotoxicity in neurodegenerative disorders (Lin and Sibille, 2013; Zhang et al., 2016). Our analysis determined that several genes important for migration, synaptogenesis, axon outgrowth and ion channel function were differentially expressed by more mature interneurons. None of the differentially expressed genes were previously shown to play a specific role in SST interneuron differentiation, though a number of them play a role in interneuron migration or differentiation in general. Disabled-1 (DAB1), has been implicated in interneuron migration, though it may not be required for this process (Hammond et al., 2006; Pla et al., 2006). Deletion of contactin-associated protein-like 2 (CNTNAP2) disrupts interneuron migration, results in a loss of interneurons, and mutations in CNTNAP2 are associated with epilepsy and autism in humans (Penagarikano et al., 2011). Calcium/calmodulin-dependent 3′,5′ cyclic nucleotide phosphodiesterase 1A (PDE1A) was recently identified as a
