Very low-depth sequencing in a founder population identifies a cardioprotective APOC3 signal missed by genome-wide imputation

Hum Mol Genet. 2016 Jun 1;25(11):2360-2365. doi: 10.1093/hmg/ddw088. Epub 2016 May 4.

Abstract

Cohort-wide very low-depth whole-genome sequencing (WGS) can comprehensively capture low-frequency sequence variation for the cost of a dense genome-wide genotyping array. Here, we analyse 1x sequence data across the APOC3 gene in a founder population from the island of Crete in Greece (n = 1239) and find significant evidence for association with blood triglyceride levels with the previously reported R19X cardioprotective null mutation (β = -1.09,σ = 0.163, P = 8.2 × 10-11) and a second loss of function mutation, rs138326449 (β = -1.17,σ = 0.188, P = 1.14 × 10-9). The signal cannot be recapitulated by imputing genome-wide genotype data on a large reference panel of 5122 individuals including 249 with 4x WGS data from the same population. Gene-level meta-analysis with other studies reporting burden signals at APOC3 provides robust evidence for a replicable cardioprotective rare variant aggregation (P = 3.2 × 10-31, n = 13 480).

Publication types

  • Meta-Analysis

MeSH terms

  • Alleles
  • Apolipoprotein C-III / genetics*
  • Cardiovascular Diseases / blood
  • Cardiovascular Diseases / genetics*
  • Cardiovascular Diseases / pathology
  • Female
  • Founder Effect
  • Genetics, Population
  • Genome, Human
  • Genome-Wide Association Study
  • Genotype
  • Greece
  • High-Throughput Nucleotide Sequencing*
  • Humans
  • Male
  • Mutation
  • Polymorphism, Single Nucleotide
  • Triglycerides / blood
  • Triglycerides / genetics*
  • White People / genetics

Substances

  • Apolipoprotein C-III
  • Triglycerides