A genomic prediction model for racecourse starts in the Thoroughbred horse
Summary Durability traits in Thoroughbred horses are heritable, economically valuable and may affect horse welfare. The aims of this study were to test the hypotheses that (i) durability traits are heritable and (ii) genetic data may be used to predict a horse's potential to have a racecourse s...
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Veröffentlicht in: | Animal genetics 2019-08, Vol.50 (4), p.347-357 |
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creator | McGivney, B. A. Hernandez, B. Katz, L. M. MacHugh, D. E. McGovern, S. P. Parnell, A. C. Wiencko, H. L. Hill, E. W. |
description | Summary
Durability traits in Thoroughbred horses are heritable, economically valuable and may affect horse welfare. The aims of this study were to test the hypotheses that (i) durability traits are heritable and (ii) genetic data may be used to predict a horse's potential to have a racecourse start. Heritability for the phenotype ‘number of 2‐ and 3‐year‐old starts’ was estimated to be hm2 = 0.11 ± 0.02 (n = 4499). A genome‐wide association study identified SNP contributions to the trait. The neurotrimin (NTM), opioid‐binding protein/cell adhesion molecule like (OPCML) and prolylcarboxypeptidase (PRCP) genes were identified as candidate genes associated with the trait. NTM functions in brain development and has been shown to have been selected during the domestication of the horse. PRCP is an established expression quantitative trait locus involved in the interaction between voluntary exercise and body composition in mice. We hypothesise that variation at these loci contributes to the motivation of the horse to exercise, which may influence its response to the demands of the training and racing environment. A random forest with mixed effects (RFME) model identified a set of SNPs that contributed to 24.7% of the heritable variation in the trait. In an independent validation set (n = 528 horses), the cohort with high genetic potential for a racecourse start had significantly fewer unraced horses (16% unraced) than did low (27% unraced) potential horses and had more favourable race outcomes among those that raced. Therefore, the information from SNPs included in the model may be used to predict horses with a greater chance of a racecourse start. |
doi_str_mv | 10.1111/age.12798 |
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Durability traits in Thoroughbred horses are heritable, economically valuable and may affect horse welfare. The aims of this study were to test the hypotheses that (i) durability traits are heritable and (ii) genetic data may be used to predict a horse's potential to have a racecourse start. Heritability for the phenotype ‘number of 2‐ and 3‐year‐old starts’ was estimated to be hm2 = 0.11 ± 0.02 (n = 4499). A genome‐wide association study identified SNP contributions to the trait. The neurotrimin (NTM), opioid‐binding protein/cell adhesion molecule like (OPCML) and prolylcarboxypeptidase (PRCP) genes were identified as candidate genes associated with the trait. NTM functions in brain development and has been shown to have been selected during the domestication of the horse. PRCP is an established expression quantitative trait locus involved in the interaction between voluntary exercise and body composition in mice. We hypothesise that variation at these loci contributes to the motivation of the horse to exercise, which may influence its response to the demands of the training and racing environment. A random forest with mixed effects (RFME) model identified a set of SNPs that contributed to 24.7% of the heritable variation in the trait. In an independent validation set (n = 528 horses), the cohort with high genetic potential for a racecourse start had significantly fewer unraced horses (16% unraced) than did low (27% unraced) potential horses and had more favourable race outcomes among those that raced. Therefore, the information from SNPs included in the model may be used to predict horses with a greater chance of a racecourse start.</description><identifier>ISSN: 0268-9146</identifier><identifier>EISSN: 1365-2052</identifier><identifier>DOI: 10.1111/age.12798</identifier><identifier>PMID: 31257665</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>behaviour ; Body composition ; Brain ; Cell adhesion ; Cell adhesion & migration ; Cell adhesion molecules ; Domestication ; Durability ; equine ; Gene mapping ; Genes ; Genome-wide association studies ; Genomes ; genome‐wide association study ; Heritability ; Horse racing ; Horses ; Lysosomal Pro-X carboxypeptidase ; Motivation ; Opioids ; Phenotypes ; Prediction models ; Quantitative trait loci ; Racehorses ; random forest model ; Single-nucleotide polymorphism ; temperament</subject><ispartof>Animal genetics, 2019-08, Vol.50 (4), p.347-357</ispartof><rights>2019 Stichting International Foundation for Animal Genetics</rights><rights>2019 Stichting International Foundation for Animal Genetics.</rights><rights>Copyright © 2019 Stichting International Foundation for Animal Genetics</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3888-3e4b9397b20f5302ec547336cbd903fa526a323f7503a7d7603718c029de83303</citedby><cites>FETCH-LOGICAL-c3888-3e4b9397b20f5302ec547336cbd903fa526a323f7503a7d7603718c029de83303</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fage.12798$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fage.12798$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27902,27903,45552,45553</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31257665$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McGivney, B. A.</creatorcontrib><creatorcontrib>Hernandez, B.</creatorcontrib><creatorcontrib>Katz, L. M.</creatorcontrib><creatorcontrib>MacHugh, D. E.</creatorcontrib><creatorcontrib>McGovern, S. P.</creatorcontrib><creatorcontrib>Parnell, A. C.</creatorcontrib><creatorcontrib>Wiencko, H. L.</creatorcontrib><creatorcontrib>Hill, E. W.</creatorcontrib><title>A genomic prediction model for racecourse starts in the Thoroughbred horse</title><title>Animal genetics</title><addtitle>Anim Genet</addtitle><description>Summary
Durability traits in Thoroughbred horses are heritable, economically valuable and may affect horse welfare. The aims of this study were to test the hypotheses that (i) durability traits are heritable and (ii) genetic data may be used to predict a horse's potential to have a racecourse start. Heritability for the phenotype ‘number of 2‐ and 3‐year‐old starts’ was estimated to be hm2 = 0.11 ± 0.02 (n = 4499). A genome‐wide association study identified SNP contributions to the trait. The neurotrimin (NTM), opioid‐binding protein/cell adhesion molecule like (OPCML) and prolylcarboxypeptidase (PRCP) genes were identified as candidate genes associated with the trait. NTM functions in brain development and has been shown to have been selected during the domestication of the horse. PRCP is an established expression quantitative trait locus involved in the interaction between voluntary exercise and body composition in mice. We hypothesise that variation at these loci contributes to the motivation of the horse to exercise, which may influence its response to the demands of the training and racing environment. A random forest with mixed effects (RFME) model identified a set of SNPs that contributed to 24.7% of the heritable variation in the trait. In an independent validation set (n = 528 horses), the cohort with high genetic potential for a racecourse start had significantly fewer unraced horses (16% unraced) than did low (27% unraced) potential horses and had more favourable race outcomes among those that raced. Therefore, the information from SNPs included in the model may be used to predict horses with a greater chance of a racecourse start.</description><subject>behaviour</subject><subject>Body composition</subject><subject>Brain</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell adhesion molecules</subject><subject>Domestication</subject><subject>Durability</subject><subject>equine</subject><subject>Gene mapping</subject><subject>Genes</subject><subject>Genome-wide association studies</subject><subject>Genomes</subject><subject>genome‐wide association study</subject><subject>Heritability</subject><subject>Horse racing</subject><subject>Horses</subject><subject>Lysosomal Pro-X carboxypeptidase</subject><subject>Motivation</subject><subject>Opioids</subject><subject>Phenotypes</subject><subject>Prediction models</subject><subject>Quantitative trait loci</subject><subject>Racehorses</subject><subject>random forest model</subject><subject>Single-nucleotide polymorphism</subject><subject>temperament</subject><issn>0268-9146</issn><issn>1365-2052</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp10LtOwzAUBmALgaBcBl4AWWKBIcWX-pKxqspNlVjKbDnOSRuUxMVOhHh7TFsYkPByPHz-dfwjdEnJmKZzZ1cwpkzl-gCNKJciY0SwQzQiTOospxN5gk5jfCOEaKroMTrhlAklpRih5yleQefb2uFNgLJ2fe073PoSGlz5gIN14PwQIuDY29BHXHe4XwNern3ww2pdpFc43SOco6PKNhEu9vMMvd7Pl7PHbPHy8DSbLjLHtdYZh0mR81wVjFSCEwZOTBTn0hVlTnhlBZOWM14pQbhVpZKEK6odYXkJmnPCz9DNLncT_PsAsTdtHR00je3AD9EwJohkIqcs0es_9C39pUvbbZWY5FSrpG53ygUfY4DKbELd2vBpKDHfBZtUsNkWnOzVPnEoWih_5U-jCdztwEfdwOf_SWb6MN9FfgG6FIIc</recordid><startdate>201908</startdate><enddate>201908</enddate><creator>McGivney, B. A.</creator><creator>Hernandez, B.</creator><creator>Katz, L. M.</creator><creator>MacHugh, D. E.</creator><creator>McGovern, S. P.</creator><creator>Parnell, A. C.</creator><creator>Wiencko, H. L.</creator><creator>Hill, E. W.</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>201908</creationdate><title>A genomic prediction model for racecourse starts in the Thoroughbred horse</title><author>McGivney, B. A. ; Hernandez, B. ; Katz, L. M. ; MacHugh, D. E. ; McGovern, S. P. ; Parnell, A. C. ; Wiencko, H. L. ; Hill, E. W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3888-3e4b9397b20f5302ec547336cbd903fa526a323f7503a7d7603718c029de83303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>behaviour</topic><topic>Body composition</topic><topic>Brain</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell adhesion molecules</topic><topic>Domestication</topic><topic>Durability</topic><topic>equine</topic><topic>Gene mapping</topic><topic>Genes</topic><topic>Genome-wide association studies</topic><topic>Genomes</topic><topic>genome‐wide association study</topic><topic>Heritability</topic><topic>Horse racing</topic><topic>Horses</topic><topic>Lysosomal Pro-X carboxypeptidase</topic><topic>Motivation</topic><topic>Opioids</topic><topic>Phenotypes</topic><topic>Prediction models</topic><topic>Quantitative trait loci</topic><topic>Racehorses</topic><topic>random forest model</topic><topic>Single-nucleotide polymorphism</topic><topic>temperament</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McGivney, B. A.</creatorcontrib><creatorcontrib>Hernandez, B.</creatorcontrib><creatorcontrib>Katz, L. M.</creatorcontrib><creatorcontrib>MacHugh, D. E.</creatorcontrib><creatorcontrib>McGovern, S. P.</creatorcontrib><creatorcontrib>Parnell, A. C.</creatorcontrib><creatorcontrib>Wiencko, H. L.</creatorcontrib><creatorcontrib>Hill, E. W.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Animal genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McGivney, B. A.</au><au>Hernandez, B.</au><au>Katz, L. M.</au><au>MacHugh, D. E.</au><au>McGovern, S. P.</au><au>Parnell, A. C.</au><au>Wiencko, H. L.</au><au>Hill, E. W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A genomic prediction model for racecourse starts in the Thoroughbred horse</atitle><jtitle>Animal genetics</jtitle><addtitle>Anim Genet</addtitle><date>2019-08</date><risdate>2019</risdate><volume>50</volume><issue>4</issue><spage>347</spage><epage>357</epage><pages>347-357</pages><issn>0268-9146</issn><eissn>1365-2052</eissn><abstract>Summary
Durability traits in Thoroughbred horses are heritable, economically valuable and may affect horse welfare. The aims of this study were to test the hypotheses that (i) durability traits are heritable and (ii) genetic data may be used to predict a horse's potential to have a racecourse start. Heritability for the phenotype ‘number of 2‐ and 3‐year‐old starts’ was estimated to be hm2 = 0.11 ± 0.02 (n = 4499). A genome‐wide association study identified SNP contributions to the trait. The neurotrimin (NTM), opioid‐binding protein/cell adhesion molecule like (OPCML) and prolylcarboxypeptidase (PRCP) genes were identified as candidate genes associated with the trait. NTM functions in brain development and has been shown to have been selected during the domestication of the horse. PRCP is an established expression quantitative trait locus involved in the interaction between voluntary exercise and body composition in mice. We hypothesise that variation at these loci contributes to the motivation of the horse to exercise, which may influence its response to the demands of the training and racing environment. A random forest with mixed effects (RFME) model identified a set of SNPs that contributed to 24.7% of the heritable variation in the trait. In an independent validation set (n = 528 horses), the cohort with high genetic potential for a racecourse start had significantly fewer unraced horses (16% unraced) than did low (27% unraced) potential horses and had more favourable race outcomes among those that raced. Therefore, the information from SNPs included in the model may be used to predict horses with a greater chance of a racecourse start.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31257665</pmid><doi>10.1111/age.12798</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | behaviour Body composition Brain Cell adhesion Cell adhesion & migration Cell adhesion molecules Domestication Durability equine Gene mapping Genes Genome-wide association studies Genomes genome‐wide association study Heritability Horse racing Horses Lysosomal Pro-X carboxypeptidase Motivation Opioids Phenotypes Prediction models Quantitative trait loci Racehorses random forest model Single-nucleotide polymorphism temperament |
title | A genomic prediction model for racecourse starts in the Thoroughbred horse |
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