Gene-based analyses identified 42 significantly associated genes (Supplemental Table 3); the most significant signals were FTO (p=1.86E-13), DRD2 (p=7.9e-12), and PDE4B (p=9.63E-11). Fine-mapping identified 123 GWS SNPs (of 660 non-independent GWS SNPs) in credible sets as potential causal SNPs based on the posterior probability of inclusion (Supplemental Table 4). Mapping the lead independent SNPs in the credible sets to their nearest gene based on posterior probability of 1, the following SNPs showed the strongest causal potential: rs1937455 (PDE4B), rs3739095 (GTF3C2), rs6718128 (ZNF512), rs4143308 (RP11–89K21.1), rs4953152 (SIX3), rs41335055 (CTD-2026C7.1), rs2678900 (VRK2), rs7620024 (TCTA), rs283412 (ADH1C), rs901406 (BANK1), rs359590 (RABEPK), rs10083370 (LINC00637), rs1477196 (FTO), rs291699 (CDK5RAP1) (Supplemental Table 4 and Figure 1). Pathway analysis of gene-based results revealed several significant GO terms including double-stranded DNA binding (pbonferroni=0.005), sequence-specific double-stranded DNA binding (pbonferroni=0.01), regulation of nervous system development (2 terms: pbonferroni=0.011 – 0.037), and positive regulation of transcription by RNA polymerase (pbonferroni=0.038) (Supplemental Table 6).
