Genome-wide association study of opioid dependence: multiple associations mapped to calcium and potassium pathways.
paper
Primary
Public
- Authors
- Gelernter, Joel; Kranzler, Henry R; Sherva, Richard; Koesterer, Ryan; Almasy, Laura; Zhao, Hongyu; Farrer, Lindsay A
- Year
- 2014
- Journal
- Biological psychiatry
- PMID
- 24143882
- DOI
- 10.1016/j.biopsych.2013.08.034
- PMCID
- PMC3992201
BACKGROUND: We report a genome-wide association study (GWAS) of two populations, African-American and European-American (AA, EA) for opioid dependence (OD) in three sets of subjects, to identify pathways, genes, and alleles important in OD risk. METHODS: The design employed three phases (on the basis of separate sample collections). Phase 1 included our discovery GWAS dataset consisting of 5697 subjects (58% AA) diagnosed with opioid and/or other substance dependence and control subjects. Subjects were genotyped with the Illumina OmniQuad microarray, yielding 890,000 single nucleotide polymorphisms (SNPs) suitable for analysis. Additional genotypes were imputed with the 1000 Genomes reference panel. Top-ranked findings were further evaluated in Phase 2 by incorporating information from the publicly available Study of Addiction: Genetics and Environment dataset, with GWAS data from 4063 subjects (32% AA). In Phase 3, the most significant SNPs from Phase 2 were genotyped in 2549 independent subjects (32% AA). Analyses were performed with case-control and ordinal trait designs. RESULTS: Most significant results emerged from the AA subgroup. Genome-wide-significant associations (p < 5.0 Γ 10(-8)) were observed with SNPs from multiple loci-KCNG2*rs62103177 was most significant after combining results from datasets in every phase of the study. The most compelling results were obtained with genes involved in potassium signaling pathways (e.g., KCNC1 and KCNG2). Pathway analysis also implicated genes involved in calcium signaling and long-term potentiation. CONCLUSIONS: This is the first study to identify risk variants for OD with GWAS. Our results strongly implicate risk pathways and provide insights into novel therapeutic and prevention strategies and might biologically bridge OD and other non-substance dependence psychiatric traits where similar pathways have been implicated.
Regional association (Manhattan) plot showing Phase 1+2 meta-analyzed results for association of Sympcountadj with SNPs mapped to the KCNG2 region on chromosome 18 in the AA population. The SNPs are color coded according to r2 with the most significant SNP shown in purple. The SNP with the strongest evidence for association is shown twice: once with the Phase 1+2 meta-analysis p-value (purple with βcrosshairsβ) and once after the inclusion of the Phase 3 samples (purple without βcrosshairsβ). (They are nearly superimposed in this figure.) The light blue line and right Y-axis show the observed recombination rate in the HapMap YRI samples.
The role of genes identified in GWAS of Phase 1+2 AA subjects using a case-control model in the canonical pathway βcalcium signaling.β The gene or gene families with a significant association result are shown in orange. The calcineurin family was identified by an association in PPP3CA, the CREB family by CREB5, the HDAC family by HDAC9, and the CAMK2 family by CAMK2B (see table βpathway SNPsβ). For a full description of the functional relationships represented by the various lines and arrows, see:http://www.biolreprod.org/content/suppl/2010/09/29/biolreprod.110.085910.DC1/biolreprod.110.085910-3.pdf.
The role of genes identified in GWAS of Phase 1+2 AA subjects using a case-control model in the canonical pathway βsynaptic long-term potentiation.β The gene or gene families with a significant association result are shown in orange. The calcineurin family was identified by an association in PPP3CA, the CREB family by CREB5, and the CAMK2 family by CAMK2B (see table βpathway SNPsβ). For a full description of the functional relationships represented by the various lines and arrows, see:http://www.biolreprod.org/content/suppl/2010/09/29/biolreprod.110.085910.DC1/biolreprod.110.085910-3.pdf.
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