Genome partitioning of genetic variation for height from 11,214 sibling pairs

Visscher, Peter M., Macgregor, Stuart, Benyamin, Beben, Zhu, Gu, Gordon, Scott, Medland, Sarah, Hill, William G., Hottenga, Jouke-Jan, Willemsen, Gonneke, Boomsma, Dorret I., Liu, Yao-Zhong, Deng, Hong-Wen, Montgomery, Grant W. and Martin, Nicholas G. (2007) Genome partitioning of genetic variation for height from 11,214 sibling pairs. American Journal of Human Genetics, 81 5: 1104-1110. doi:10.1086/522934


Author Visscher, Peter M.
Macgregor, Stuart
Benyamin, Beben
Zhu, Gu
Gordon, Scott
Medland, Sarah
Hill, William G.
Hottenga, Jouke-Jan
Willemsen, Gonneke
Boomsma, Dorret I.
Liu, Yao-Zhong
Deng, Hong-Wen
Montgomery, Grant W.
Martin, Nicholas G.
Title Genome partitioning of genetic variation for height from 11,214 sibling pairs
Journal name American Journal of Human Genetics   Check publisher's open access policy
ISSN 0002-9297
Publication date 2007-11
Sub-type Article (original research)
DOI 10.1086/522934
Volume 81
Issue 5
Start page 1104
End page 1110
Total pages 7
Place of publication Chicago, United States
Publisher University of Chicago Press
Collection year 2008
Language eng
Subject 321011 Medical Genetics
730107 Inherited diseases (incl. gene therapy)
C1
Abstract Height has been used for more than a century as a model by which to understand quantitative genetic variation in humans. We report that the entire genome appears to contribute to its additive genetic variance. We used genotypes and phenotypes of 11,214 sibling pairs from three countries to partition additive genetic variance across the genome. Using genome scans to estimate the proportion of the genomes of each chromosome from siblings that were identical by descent, we estimated the heritability of height contributed by each of the 22 autosomes and the X chromosome. We show that additive genetic variance is spread across multiple chromosomes and that at least six chromosomes (i.e., 3, 4, 8, 15, 17, and 18) are responsible for the observed variation. Indeed, the data are not inconsistent with a uniform spread of trait loci throughout the genome. Our estimate of the variance explained by a chromosome is correlated with the number of times suggestive or significant linkage with height has been reported for that chromosome. Variance due to dominance was not significant but was difficult to assess because of the high sampling correlation between additive and dominance components. Results were consistent with the absence of any large between-chromosome epistatic effects. Notwithstanding the proposed architecture of complex traits that involves widespread gene-gene and gene-environment interactions, our results suggest that variation in height in humans can be explained by many loci distributed over all autosomes, with an additive mode of gene action.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status Non-UQ

 
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Created: Mon, 03 Mar 2008, 11:30:48 EST