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dc.contributor.authorPurfield, Deirdre C
dc.contributor.authorEvans, Ross D
dc.contributor.authorBerry, Donagh
dc.date.accessioned2021-01-11T17:32:08Z
dc.date.available2021-01-11T17:32:08Z
dc.date.issued2020-05-04
dc.identifier.citationDeirdre C Purfield, Ross D Evans, Donagh P Berry, Breed- and trait-specific associations define the genetic architecture of calving performance traits in cattle, Journal of Animal Science, Volume 98, Issue 5, May 2020, skaa151, https://doi.org/10.1093/jas/skaa151en_US
dc.identifier.issn0021-8812
dc.identifier.urihttp://hdl.handle.net/11019/2362
dc.descriptionpeer-revieweden_US
dc.description.abstractReducing the incidence of both the degree of assistance required at calving, as well as the extent of perinatal mortality (PM) has both economic and societal benefits. The existence of heritable genetic variability in both traits signifies the presence of underlying genomic variability. The objective of the present study was to locate regions of the genome, and by extension putative genes and mutations, that are likely to be underpinning the genetic variability in direct calving difficulty (DCD), maternal calving difficulty (MCD), and PM. Imputed whole-genome single-nucleotide polymorphism (SNP) data on up to 8,304 Angus (AA), 17,175 Charolais (CH), 16,794 Limousin (LM), and 18,474 Holstein-Friesian (HF) sires representing 5,866,712 calving events from descendants were used. Several putative quantitative trait loci (QTL) regions associated with calving performance both within and across dairy and beef breeds were identified, although the majority were both breed- and trait-specific. QTL surrounding and encompassing the myostatin (MSTN) gene were associated (P < 5 × 10−8) with DCD and PM in both the CH and LM populations. The well-known Q204X mutation was the fifth strongest association with DCD in the CH population and accounted for 5.09% of the genetic variance in DCD. In contrast, none of the 259 segregating variants in MSTN were associated (P > × 10−6) with DCD in the LM population but a genomic region 617 kb downstream of MSTN was associated (P < 5 × 10−8). The genetic architecture for DCD differed in the HF population relative to the CH and LM, where two QTL encompassing ZNF613 on Bos taurus autosome (BTA)18 and PLAG1 on BTA14 were identified in the former. Pleiotropic SNP associated with all three calving performance traits were also identified in the three beef breeds; 5 SNP were pleiotropic in AA, 116 in LM, and 882 in CH but no SNP was associated with more than one trait within the HF population. The majority of these pleiotropic SNP were on BTA2 surrounding MSTN and were associated with both DCD and PM. Multiple previously reported, but also novel QTL, associated with calving performance were detected in this large study. These also included QTL regions harboring SNP with the same direction of allele substitution effect for both DCD and MCD thus contributing to a more effective simultaneous selection for both traits.en_US
dc.description.sponsorshipScience Foundation Ireland
dc.language.isoenen_US
dc.publisherOxford University Press (OUP)en_US
dc.relation.ispartofseriesJournal of Animal Science;vol 98
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectcalving difficultyen_US
dc.subjectgenome-wide associationen_US
dc.subjectmortalityen_US
dc.subjectpleiotropyen_US
dc.subjectsequenceen_US
dc.subjectsingle-nucleotide polymorphismen_US
dc.titleBreed- and trait-specific associations define the genetic architecture of calving performance traits in cattleen_US
dc.typeArticleen_US
dc.identifier.doihttps://doi.org/10.1093/jas/skaa151
dc.contributor.sponsorEuropean Unionen_US
dc.contributor.sponsorScience Foundation Irelanden_US
dc.contributor.sponsorGrantNumber727213en_US
dc.contributor.sponsorGrantNumber14/IA/2576)en_US
dc.contributor.sponsorGrantNumber16/RC/3835en_US
dc.source.volume98
dc.source.issue5
refterms.dateFOA2021-01-11T17:32:09Z
dc.source.journaltitleJournal of Animal Science
dc.identifier.eissn1525-3163


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