4D), including KCND2, KCNJ9, KCNK9 and KCNA3, as well as a number of transcripts associated with synaptic development and function (Figure 4E and Table S2). The latter included NXPH1, NLGN3, and LINGO1, among others (Table S3, and Figures S3 and S4), synaptic genes whose dysregulation has been previously linked to both SCZ and the autism spectrum disorders (Andrews and Fernandez-Enright, 2015; Fernandez-Enright et al., 2014; Mackowiak et al., 2014; Salyakina et al., 2011; Sudhof, 2008). Whereas the expression of these latter genes was suppressed in hGPCs derived from all 4 SCZ patients, other synapse-associated genes, such as NRXN1, NLGN1, DSCAML1, and the SLITRKs 2–5, were sharply down-regulated in hGPCs derived from 3 of the 4 patients, but not in the fourth (Table S3). Yet other synapse-associated transcripts, like NXPH3 and NTRNG2, were similarly down-regulated in some patients, but not others. TaqMan low density arrays were used for quantitative real-time PCR validation of these and other dysregulated transcripts of interest, and confirmed the significant differential down-regulation of these differentiation and synaptic function-associated genes (Figure 5).
