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Genome-wide aggregated trans-effects on risk of type 1 diabetes: A test of the "omnigenic" sparse effector hypothesis of complex trait genetics.

Iakovliev A, McGurnaghan SJ, Hayward C et al.

37164005 PubMed ID
GWAS Study Type
12461 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

IA
Iakovliev A
MS
McGurnaghan SJ
HC
Hayward C
CM
Colombo M
LD
Lipschutz D
SA
Spiliopoulou A
CH
Colhoun HM
MP
McKeigue PM
Chapter II

Abstract

Summary of the research findings

The "omnigenic" hypothesis postulates that the polygenic effects of common SNPs on a typical complex trait are mediated through trans-effects on expression of a relatively sparse set of effector ("core") genes. We tested this hypothesis in a study of 4,964 cases of type 1 diabetes (T1D) and 7,497 controls by using summary statistics to calculate aggregated (excluding the HLA region) trans-scores for gene expression in blood. From associations of T1D with aggregated trans-scores, nine putative core genes were identified, of which three-STAT1, CTLA4 and FOXP3-are genes in which variants cause monogenic forms of autoimmune diabetes. Seven of these genes affect the activity of regulatory T cells, and two are involved in immune responses to microbial lipids. Four T1D-associated genomic regions could be identified as master regulators via trans-effects on gene expression. These results support the sparse effector hypothesis and reshape our understanding of the genetic architecture of T1D.

4,964 cases, 7,497 controls

Chapter III

Study Statistics

Key metrics and study information

12461
Total Participants
GWAS
Study Type
No
Replicated
U.K.
Recruitment Country
Chapter IV

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