We used qRT-PCR to validate the RNA-seq differential gene expression profile for 6 genes (Fig. 2a). Two of the selected genes map to the 22q11.2 deleted region – DGCR8 and SLC25A1. Both showed a statistically significant, ~2-fold decrease in expression, supporting the RNA-seq findings for these genes. The others were analyzed because of their relevance to SZ and our findings in pathway analysis. These included IFITM3, SSTR2, GRIK1, and MAP3K7. IFITM3 codes for interferon-induced transmembrane protein 3, which plays a role in interferon-signaling and the innate defense against influenza and other viruses [72–74]. This is interesting from a SZ pathogenesis perspective, considering the clinical and epidemiological evidence pointing towards prenatal influenza as a risk factor in SZ [75, 76]. SSTR2, which codes for somatostatin receptor 2, is important because reduced expression in the cortex, and a reduction in somatostatin positive GABAergic hippocampal neurons has been detected in SZ brains [77–79]. Finally, GRIK1, which codes for a kainite glutamate ionotropic receptor, is expressed at lower levels in SZ brains [80]. As seen in Fig. 2a, the significant changes in expression found by RNA-seq were confirmed by qPCR.
