Genome-wide Analysis of Body Proportion Classifies Height-Associated Variants by Mechanism of Action and Implicates Genes Important for Skeletal Development
Human height is a composite measurement, reflecting the sum of leg, spine, and head lengths. Many common variants influence total height, but the effects of these or other variants on the components of height (body proportion) remain largely unknown. We studied sitting height ratio (SHR), the ratio...
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| Veröffentlicht in: | American journal of human genetics Jg. 96; H. 5; S. 695 |
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| Abstract | Human height is a composite measurement, reflecting the sum of leg, spine, and head lengths. Many common variants influence total height, but the effects of these or other variants on the components of height (body proportion) remain largely unknown. We studied sitting height ratio (SHR), the ratio of sitting height to total height, to identify such effects in 3,545 African Americans and 21,590 individuals of European ancestry. We found that SHR is heritable: 26% and 39% of the total variance of SHR can be explained by common variants in European and African Americans, respectively, and global European admixture is negatively correlated with SHR in African Americans (r(2) ≈ 0.03). Six regions reached genome-wide significance (p < 5 × 10(-8)) for association with SHR and overlapped biological candidate genes, including TBX2 and IGFBP3. We found that 130 of 670 height-associated variants are nominally associated (p < 0.05) with SHR, more than expected by chance (p = 5 × 10(-40)). At these 130 loci, the height-increasing alleles are associated with either a decrease (71 loci) or increase (59 loci) in SHR, suggesting that different height loci disproportionally affect either leg length or spine/head length. Pathway analyses via DEPICT revealed that height loci affecting SHR, and especially those affecting leg length, show enrichment of different biological pathways (e.g., bone/cartilage/growth plate pathways) than do loci with no effect on SHR (e.g., embryonic development). These results highlight the value of using a pair of related but orthogonal phenotypes, in this case SHR with height, as a prism to dissect the biology underlying genetic associations in polygenic traits and diseases. |
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| AbstractList | Human height is a composite measurement, reflecting the sum of leg, spine, and head lengths. Many common variants influence total height, but the effects of these or other variants on the components of height (body proportion) remain largely unknown. We studied sitting height ratio (SHR), the ratio of sitting height to total height, to identify such effects in 3,545 African Americans and 21,590 individuals of European ancestry. We found that SHR is heritable: 26% and 39% of the total variance of SHR can be explained by common variants in European and African Americans, respectively, and global European admixture is negatively correlated with SHR in African Americans (r(2) ≈ 0.03). Six regions reached genome-wide significance (p < 5 × 10(-8)) for association with SHR and overlapped biological candidate genes, including TBX2 and IGFBP3. We found that 130 of 670 height-associated variants are nominally associated (p < 0.05) with SHR, more than expected by chance (p = 5 × 10(-40)). At these 130 loci, the height-increasing alleles are associated with either a decrease (71 loci) or increase (59 loci) in SHR, suggesting that different height loci disproportionally affect either leg length or spine/head length. Pathway analyses via DEPICT revealed that height loci affecting SHR, and especially those affecting leg length, show enrichment of different biological pathways (e.g., bone/cartilage/growth plate pathways) than do loci with no effect on SHR (e.g., embryonic development). These results highlight the value of using a pair of related but orthogonal phenotypes, in this case SHR with height, as a prism to dissect the biology underlying genetic associations in polygenic traits and diseases.Human height is a composite measurement, reflecting the sum of leg, spine, and head lengths. Many common variants influence total height, but the effects of these or other variants on the components of height (body proportion) remain largely unknown. We studied sitting height ratio (SHR), the ratio of sitting height to total height, to identify such effects in 3,545 African Americans and 21,590 individuals of European ancestry. We found that SHR is heritable: 26% and 39% of the total variance of SHR can be explained by common variants in European and African Americans, respectively, and global European admixture is negatively correlated with SHR in African Americans (r(2) ≈ 0.03). Six regions reached genome-wide significance (p < 5 × 10(-8)) for association with SHR and overlapped biological candidate genes, including TBX2 and IGFBP3. We found that 130 of 670 height-associated variants are nominally associated (p < 0.05) with SHR, more than expected by chance (p = 5 × 10(-40)). At these 130 loci, the height-increasing alleles are associated with either a decrease (71 loci) or increase (59 loci) in SHR, suggesting that different height loci disproportionally affect either leg length or spine/head length. Pathway analyses via DEPICT revealed that height loci affecting SHR, and especially those affecting leg length, show enrichment of different biological pathways (e.g., bone/cartilage/growth plate pathways) than do loci with no effect on SHR (e.g., embryonic development). These results highlight the value of using a pair of related but orthogonal phenotypes, in this case SHR with height, as a prism to dissect the biology underlying genetic associations in polygenic traits and diseases. Human height is a composite measurement, reflecting the sum of leg, spine, and head lengths. Many common variants influence total height, but the effects of these or other variants on the components of height (body proportion) remain largely unknown. We studied sitting height ratio (SHR), the ratio of sitting height to total height, to identify such effects in 3,545 African Americans and 21,590 individuals of European ancestry. We found that SHR is heritable: 26% and 39% of the total variance of SHR can be explained by common variants in European and African Americans, respectively, and global European admixture is negatively correlated with SHR in African Americans (r(2) ≈ 0.03). Six regions reached genome-wide significance (p < 5 × 10(-8)) for association with SHR and overlapped biological candidate genes, including TBX2 and IGFBP3. We found that 130 of 670 height-associated variants are nominally associated (p < 0.05) with SHR, more than expected by chance (p = 5 × 10(-40)). At these 130 loci, the height-increasing alleles are associated with either a decrease (71 loci) or increase (59 loci) in SHR, suggesting that different height loci disproportionally affect either leg length or spine/head length. Pathway analyses via DEPICT revealed that height loci affecting SHR, and especially those affecting leg length, show enrichment of different biological pathways (e.g., bone/cartilage/growth plate pathways) than do loci with no effect on SHR (e.g., embryonic development). These results highlight the value of using a pair of related but orthogonal phenotypes, in this case SHR with height, as a prism to dissect the biology underlying genetic associations in polygenic traits and diseases. |
| Author | Hsu, Yu-Han H Franke, Lude Smith, George Davey Pers, Tune H Hirschhorn, Joel N Esko, Tonu Strachan, David P Chan, Yingleong Salem, Rany M Vedantam, Sailaja Guo, Michael H McMahon, George Lim, Elaine T |
| Author_xml | – sequence: 1 givenname: Yingleong surname: Chan fullname: Chan, Yingleong email: rigel@broadinstitute.org organization: Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of the Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA; Divisions of Endocrinology and Genetics and Center for Basic and Translational Obesity Research, Boston Children's Hospital, Boston, MA 02115, USA; Wyss Institute for Biologically Inspired Engineering, Harvard Medical School, Boston, MA 02115, USA. Electronic address: rigel@broadinstitute.org – sequence: 2 givenname: Rany M surname: Salem fullname: Salem, Rany M organization: Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of the Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA; Divisions of Endocrinology and Genetics and Center for Basic and Translational Obesity Research, Boston Children's Hospital, Boston, MA 02115, USA – sequence: 3 givenname: Yu-Han H surname: Hsu fullname: Hsu, Yu-Han H organization: Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of the Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA; Divisions of Endocrinology and Genetics and Center for Basic and Translational Obesity Research, Boston Children's Hospital, Boston, MA 02115, USA – sequence: 4 givenname: George surname: McMahon fullname: McMahon, George organization: School of Social and Community Medicine, University of Bristol, Oakfield House, Oakfield Grove, Bristol BS8 2BN, UK – sequence: 5 givenname: Tune H surname: Pers fullname: Pers, Tune H organization: Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of the Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA; Divisions of Endocrinology and Genetics and Center for Basic and Translational Obesity Research, Boston Children's Hospital, Boston, MA 02115, USA – sequence: 6 givenname: Sailaja surname: Vedantam fullname: Vedantam, Sailaja organization: Broad Institute of the Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA; Divisions of Endocrinology and Genetics and Center for Basic and Translational Obesity Research, Boston Children's Hospital, Boston, MA 02115, USA – sequence: 7 givenname: Tonu surname: Esko fullname: Esko, Tonu organization: Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of the Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA; Divisions of Endocrinology and Genetics and Center for Basic and Translational Obesity Research, Boston Children's Hospital, Boston, MA 02115, USA; Estonian Genome Center, University of Tartu, Tartu 51010, Estonia – sequence: 8 givenname: Michael H surname: Guo fullname: Guo, Michael H organization: Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of the Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA; Divisions of Endocrinology and Genetics and Center for Basic and Translational Obesity Research, Boston Children's Hospital, Boston, MA 02115, USA – sequence: 9 givenname: Elaine T surname: Lim fullname: Lim, Elaine T organization: Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of the Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA; Divisions of Endocrinology and Genetics and Center for Basic and Translational Obesity Research, Boston Children's Hospital, Boston, MA 02115, USA – sequence: 10 givenname: Lude surname: Franke fullname: Franke, Lude organization: Department of Genetics, University of Groningen, University Medical Centre Groningen, Groningen 9700 AB, the Netherlands – sequence: 11 givenname: George Davey surname: Smith fullname: Smith, George Davey organization: School of Social and Community Medicine, University of Bristol, Oakfield House, Oakfield Grove, Bristol BS8 2BN, UK; MRC Integrative Epidemiology Unit, University of Bristol, Bristol BS8 2PR, UK – sequence: 12 givenname: David P surname: Strachan fullname: Strachan, David P organization: Population Health Research Institute, St George's, University of London, London SW17 0RE, UK – sequence: 13 givenname: Joel N surname: Hirschhorn fullname: Hirschhorn, Joel N email: joelh@broadinstitute.org organization: Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of the Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA; Divisions of Endocrinology and Genetics and Center for Basic and Translational Obesity Research, Boston Children's Hospital, Boston, MA 02115, USA. Electronic address: joelh@broadinstitute.org |
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| SubjectTerms | Adult Black or African American - genetics Body Height - genetics Chromosome Mapping Female Genome-Wide Association Study Humans Leg Bones - growth & development Male Middle Aged Multifactorial Inheritance - genetics Phenotype Polymorphism, Single Nucleotide White People - genetics |
| Title | Genome-wide Analysis of Body Proportion Classifies Height-Associated Variants by Mechanism of Action and Implicates Genes Important for Skeletal Development |
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