Deelnemers

Heb je een vraag? Neem gerust contact met ons op.

 

Telefoon: 050 - 36 11 113 (werkdagen van 8.00 - 17.00 uur)

Contactformulier

Researchers

Do you have a question regarding working with Lifelines? Please contact us, we're happy to help you.

Contact us

Pers

We voorzien media graag van informatie en we behandelen graag verzoeken voor interviews, opnames en beeldmateriaal.

Stuur een e-mail

Contact

Defining the role of common variation in the genomic and biological architecture of adult human height.

Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated ∼2,000, ∼3,700 and ∼9,500 SNPs explained ∼21%, ∼24% and ∼29% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/β-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants.

Year of publication

2014

Journal

Nat Genet.

Author(s)

Wood, AR
Esko, T
Yang, J
Vedantam, S
Pers, TH
Gustafsson, S
et al.

Full publication

Click here to view the full publicationClick here to view the full publication

Tags