Allele-specific transcription factor binding in liver and cervix cells unveils many likely drivers of GWAS signals

Genomics. 2016 Jun;107(6):248-54. doi: 10.1016/j.ygeno.2016.04.006. Epub 2016 Apr 26.

Abstract

Genome-wide association studies (GWAS) point to regions with associated genetic variants but rarely to a specific gene and therefore detailed knowledge regarding the genes contributing to complex traits and diseases remains elusive. The functional role of GWAS-SNPs is also affected by linkage disequilibrium with many variants on the same haplotype and sometimes in the same regulatory element almost equally likely to mediate the effect. Using ChIP-seq data on many transcription factors, we pinpointed genetic variants in HepG2 and HeLa-S3 cell lines which show a genome-wide significant difference in binding between alleles. We identified a collection of 3713 candidate functional regulatory variants many of which are likely drivers of GWAS signals or genetic difference in expression. A recent study investigated many variants before finding the functional ones at the GALNT2 locus, which we found in our genome-wide screen in HepG2. This illustrates the efficiency of our approach.

Keywords: Allele-specific regulation; Association to GWAS/eQTLs; Functional variants.

MeSH terms

  • Alleles
  • Cervix Uteri / metabolism
  • Female
  • Gene Expression / genetics
  • Genes, Regulator / genetics*
  • Genetic Predisposition to Disease*
  • Genome, Human
  • Genome-Wide Association Study*
  • Haplotypes
  • HeLa Cells
  • Hep G2 Cells
  • Humans
  • Linkage Disequilibrium
  • Liver / metabolism
  • N-Acetylgalactosaminyltransferases / biosynthesis
  • N-Acetylgalactosaminyltransferases / genetics
  • Polymorphism, Single Nucleotide
  • Polypeptide N-acetylgalactosaminyltransferase
  • Quantitative Trait Loci / genetics
  • Transcription Factors / biosynthesis
  • Transcription Factors / genetics*

Substances

  • Transcription Factors
  • N-Acetylgalactosaminyltransferases