loci for which we observed regulatory potential of GWAS variants the risk variants altered expression of only one gene. Experimental manipulation of three of these genes had an impact on neuroanatomical and developmental attributes in model systems, making these genes excellent candidates for further biological investigation. We also detected replicable differences in gene expression in SCZ that point to subtle but broad disruption in transcription, which is consistent with the polygenic nature of genetic risk underlying SCZ. Finally, we identified a subnetwork of ~1400 genes sub-serving functions related to synaptic transmission that is significantly perturbed in SCZ and is highly enriched for SCZ genetic signal.
