An Expanded View of Complex Traits: From Polygenic to Omnigenic

Boyle EA, Li YI, Pritchard JK

Published June 15, 2017 Cell
DOI 10.1016/j.cell.2017.05.038 PMID 28622505 PMC PMC5536862

Abstract

A central goal of genetics is to understand the links between genetic variation and disease. Intuitively, one might expect disease-causing variants to cluster into key pathways that drive disease etiology. But for complex traits, association signals tend to be spread across most of the genome-including near many genes without an obvious connection to disease. We propose that gene regulatory networks are sufficiently interconnected such that all genes expressed in disease-relevant cells are liable to affect the functions of core disease-related genes and that most heritability can be explained by effects on genes outside core pathways. We refer to this hypothesis as an "omnigenic" model.

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PMID 28622505 28622505 DOI 10.1016/j.cell.2017.05.038 10.1016/j.cell.2017.05.038 Boyle et al. 2017, Boyle 2017