causal variants across populations (100% vs. 70% vs. 40%); (vii) allele frequency and LD dependent genetic architecture: instead of sampling per-allele SNP effect sizes from a multivariate normal distribution with homogeneous variance across the genome, we assumed that the variance of SNP j in population k is proportional to [2fjk(1−fjk)]αℓjkα, where fjk and ℓjk are the MAF and LD score of SNP j in population k, respectively. When α < 0 , variants with lower MAF and variants located in lower LD regions tend to have larger effects on the trait46–48. We used α = −0.25 in this set of simulations, which has been empirically estimated to reflect the relationship between effect size and allele frequency46. This α value produced approximately a 4-fold difference in the variance of per-allele effect size for both high-frequency vs. low-frequency variants and high-LD vs. low-LD variants included in the simulations; (ix) varying hyper-parameters in the continuous shrinkage prior (a=0.5, b=0.5 vs. a=1.0, b=0.5 vs. a=1.5, b=0.5 vs. a=1.0, b=1.0).
