| Literature DB >> 25383972 |
Noah Zaitlen1, Bogdan Pasaniuc2, Sriram Sankararaman3, Gaurav Bhatia4, Jianqi Zhang5, Alexander Gusev4, Taylor Young6, Arti Tandon3, Samuela Pollack4, Bjarni J Vilhjálmsson4, Themistocles L Assimes7, Sonja I Berndt8, William J Blot9, Stephen Chanock8, Nora Franceschini10, Phyllis G Goodman11, Jing He5, Anselm J M Hennis12, Ann Hsing13, Sue A Ingles5, William Isaacs14, Rick A Kittles15, Eric A Klein16, Leslie A Lange17, Barbara Nemesure18, Nick Patterson6, David Reich19, Benjamin A Rybicki20, Janet L Stanford21, Victoria L Stevens22, Sara S Strom23, Eric A Whitsel10, John S Witte24, Jianfeng Xu25, Christopher Haiman26, James G Wilson27, Charles Kooperberg21, Daniel Stram5, Alex P Reiner28, Hua Tang29, Alkes L Price4.
Abstract
Despite recent progress on estimating the heritability explained by genotyped SNPs (h(2)g), a large gap between h(2)g and estimates of total narrow-sense heritability (h(2)) remains. Explanations for this gap include rare variants or upward bias in family-based estimates of h(2) due to shared environment or epistasis. We estimate h(2) from unrelated individuals in admixed populations by first estimating the heritability explained by local ancestry (h(2)γ). We show that h(2)γ = 2FSTCθ(1 - θ)h(2), where FSTC measures frequency differences between populations at causal loci and θ is the genome-wide ancestry proportion. Our approach is not susceptible to biases caused by epistasis or shared environment. We applied this approach to the analysis of 13 phenotypes in 21,497 African-American individuals from 3 cohorts. For height and body mass index (BMI), we obtained h(2) estimates of 0.55 ± 0.09 and 0.23 ± 0.06, respectively, which are larger than estimates of h(2)g in these and other data but smaller than family-based estimates of h(2).Entities:
Mesh：
Year: 2014 PMID： 25383972 PMCID： PMC4244251 DOI： 10.1038/ng.3139
Source DB: PubMed Journal: Nat Genet ISSN： 1061-4036 Impact factor: 38.330