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Common variants in FOXP1 are associated with generalized vitiligo

In a recent genome-wide association study of generalized vitiligo (GV) we identified 10 confirmed susceptibility loci. By testing additional loci that showed suggestive association in the genome-wide study, using two replication cohorts of European descent, we observed replicated association of GV with variants at 3p13 encompassing FOXP1 (rs17008723, combined P = 1.04 × 10-8) and with variants at 6q27 encompassing CCR6 (rs6902119, combined P = 3.94 × 10-7).

Written informed consent was obtained from all study subjects. This study was approved by each institutional review board and was conducted according to Declaration of Helsinki principles.

GENOTYPING AND QUALITY CONTROL
Genomic DNA was prepared from peripheral-blood specimens by standard methods or from saliva specimens with use of a DNA self-collection kit using the manufacturer's instructions (Oragene, DNA Genotek). DNA concentrations were assayed by ultraviolet A260 spectrophotometry (NanoDrop, Thermo Scientific). Genomewide genotyping and quality control filtering of the genomewide genotyping data has been described elsewhere 2 . Briefly, we initially determined genotypes for approximately 610,000 SNPs in 1514 CEU GV cases using the Illumina 610-Quad BeadChip, and compared SNP allele frequencies to those of 2813 "public" controls genotyped using the Illumina 1M BeadChip, obtained from the Databases of Genotypes and Phenotypes (dbGaP) (n = 2731) and the Illumina iControlDB (n = 82). After stringent quality control filtering of SNP data and removal of genetic outliers and unmatchable individuals after genetic matching using GEM 3 , we performed unadjusted and eigenvector-adjusted Cochran-Armitage trend tests of the remaining 520,460 SNPs in the remaining 1392 cases and 2629 controls using PLINK 4 and EIGENSTRAT 5 , correcting test statistics for the remaining genomic inflation factor of 1.048 using the genomic control method 6 .
Genotypes for additional SNPs across each of the candidate association regions were imputed from the GWA genotype dataset by use of MACH 7 , ver.1.0 (http://www.sph.umich.edu/csg/abecasis/MACH/download/), based on phased haplotype data in the HapMap 8 CEU samples (phase II release 24, and phase III release 2). Only imputed genotypes with r 2 > 0.3 were used for further analyses.
In the present replication study we successfully determined genotypes for the most significant SNP from each of the seven loci that showed suggestive association in the initial GWA analysis, defined as nominal P values better than 10 -4 for multiple SNPs across a contiguous genomic region, using the Sequenom MassArray iPLEX genotyping system. FOXP1 SNP rs17008713 could not be genotyped using the MassArray system for technical reasons; accordingly, we imputed genotypes for nearby SNP rs17008723 (imputed genotype r 2 = 0.995), which is in almost complete LD with rs17008713 in the GWA dataset (r 2 = 0.99), and in the replication study we therefore genotyped rs17008723. Family-based data were subjected to Mendelian error-checking, and incompatibilities were either resolved or the incompatible individual or entire family was excluded. Two SNPs were excluded on the basis of apparent deviation from Hardy-Weinberg equilibrium in controls.

STATISTICAL ANALYSES
Statistical analyses of the GWA study have been described in detail elsewhere 2 . In the casecontrol replication study, after quality control filtering, we compared allele frequencies for the remaining SNPs in 647 patients and 1056 controls using the Cochran-Armitage trend test 5 . Odds ratios and 95% confidence limits were calculated by logistic regression analysis. In the familybased replication study, we calculated the association of each SNP with vitiligo using the familybased association test (FBAT) 9 , version 1.5.5. Odds ratios (ORs) and 95% confidence limits were calculated by conditional logistic regression analysis, using matched case-pseudocontrol data derived from the family data 10 . To obtain combined P values and ORs, we performed metaanalysis using a Cochran-Mantel-Haenszel test with cases and controls from the GWA study and the case-control replication study, and cases and pseudocontrols derived from the family-based dataset, and with just the two replication datasets. The fraction of variance accounted for by each of the confirmed GV association signals, and by all 12 loci combined, was calculated as Pseudo R 2 by logistic regression analysis of the GWA and replication study case-control dataset using STATA, assuming a multiplicative model for each SNP 11 and a polygenic multiplicative model for all 12 loci combined 12 .
To test whether the P-values of the GV-associated CCR6 SNP rs6902119 and the Crohn's disease-associated CCR6 SNP rs2301436 were independent of each other in the vitiligo data, we   SNP rs2192346 and rs7868451 were located at nt 8,176,301in the ICA1 region of 7p21.3, and nt 100,987,622 in the TBC1D2 region of 9q22.33, respectively. SNP nucleotide positions are from GRCh37 and genes in close proximity to the designated SNP are denoted. AF RA , allele frequency of the risk allele EIGENSTRAT GWA P-values for SNPs rs2192346 and rs7868451 were 5.40 x 10 -5 , and 6.80 x 10 -5 , respectively. PLINK and EIGENSTRAT GWA test statistics were calculated and adjusted for the genomic inflation factor 1.048 as described in the Supplementary Methods. The Bonferroni adjusted significance threshold for the combined replication stage 1 + 2 meta-analysis was P < 1.00 x 10 -2 , and the significance threshold for the overall combined GWA + replication stage 1 + 2 meta-analysis was P < 5 x 10 -8 .