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Assessing the contribution of rare variants to complex trait heritability from whole-genome sequence data
Journal article   Peer reviewed

Assessing the contribution of rare variants to complex trait heritability from whole-genome sequence data

Pierrick Wainschtein, Deepti Jain, Zhili Zheng, L Adrienne Cupples, Aladdin H Shadyab, Barbara McKnight, Benjamin M Shoemaker, Braxton D Mitchell, Bruce M Psaty, Charles Kooperberg, …
Nature genetics, Vol.54(3), pp.263-273
03/2022
DOI: 10.1038/s41588-021-00997-7
PMCID: PMC9119698
PMID: 35256806
url
https://www.ncbi.nlm.nih.gov/pmc/articles/9119698View
Open Access

Abstract

Analyses of data from genome-wide association studies on unrelated individuals have shown that, for human traits and diseases, approximately one-third to two-thirds of heritability is captured by common SNPs. However, it is not known whether the remaining heritability is due to the imperfect tagging of causal variants by common SNPs, in particular whether the causal variants are rare, or whether it is overestimated due to bias in inference from pedigree data. Here we estimated heritability for height and body mass index (BMI) from whole-genome sequence data on 25,465 unrelated individuals of European ancestry. The estimated heritability was 0.68 (standard error 0.10) for height and 0.30 (standard error 0.10) for body mass index. Low minor allele frequency variants in low linkage disequilibrium (LD) with neighboring variants were enriched for heritability, to a greater extent for protein-altering variants, consistent with negative selection. Our results imply that rare variants, in particular those in regions of low linkage disequilibrium, are a major source of the still missing heritability of complex traits and disease.
Alleles Genome-Wide Association Study - methods Humans Linkage Disequilibrium Multifactorial Inheritance - genetics Polymorphism, Single Nucleotide - genetics

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