Heritability estimation of osteochondrosis dissecans in Maremmano horses

Pieramati, Camillo; Pepe, Marco; Silvestrelli, Maurizio; Bolla, A.

doi:10.1016/s0301-6226(02)00151-3

Cited by 38 publications

(29 citation statements)

References 14 publications

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“…Specific causes are still unknown but the origin of OC is multifactorial, including genetic factors, growth rate, body size, nutrition, mineral imbalance, endocrinological dysfunction and biomechanical trauma (Jeffcott, 1991;Van Weeren, 2005). The heritability estimates in animal threshold models were in the range from 0.10 to 0.34 for trotters, warmblood and coldblood horses for the prevalence of OC and these estimates corroborate the hereditary disposition to OC (Grøndahl and Dolvik, 1993;Philipsson et al, 1993;KWPN, 1994;Pieramati et al, 2003;Schober, 2003;Stock et al, 2005b;Wittwer et al, 2007a).…”

Section: Introductionsupporting

confidence: 52%

Refinement of a quantitative gene locus on equine chromosome 16 responsible for osteochondrosis in Hanoverian warmblood horses

Lampe¹,

Dierks²,

Distl³

2009

Animal

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Osteochondrosis (OC) is an inherited developmental disease in young horses most frequently observed in thoroughbreds, trotters, warmblood and coldblood horses. Quantitative trait loci (QTL) for equine OC have been identified in Hanoverian warmblood horses employing a whole genome scan with microsatellites. A QTL on ECA16 reached the genome-wide significance level for hock osteochondrosis dissecans (OCD). The aim of this study was to refine this QTL on ECA16 using an extended marker set of 34 newly developed microsatellites and 15 single nucleotide polymorphisms (SNPs). We used the same 14 paternal half-sib groups as in the above-mentioned whole genome scan. The QTL for OCD in hock joints on ECA16 could be delimited at an interval between 17.60 and 45.18 Mb using multipoint non-parametric linkage analyses. In addition, six microsatellites and one SNP were significantly associated with hock OCD in the QTL region between 24.26 and 42.41 Mb. Furthermore, our analysis revealed a second QTL for fetlock OC between 6.55 and 24.26 Mb on ECA16. This report is a further step towards unravelling the genes underlying QTL for equine OC and towards the development of a marker test for OC in Hanoverian warmblood horses.

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Section: Introductionsupporting

confidence: 52%

Refinement of a quantitative gene locus on equine chromosome 16 responsible for osteochondrosis in Hanoverian warmblood horses

Lampe¹,

Dierks²,

Distl³

2009

Animal

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“…Prevalence estimates for OC vary widely, ranging from 3% (stifle OC in Thoroughbreds (Oliver et al 2008)) to 70% (estimates for all joints in Dutch Warmbloods (van Grevenhof et al 2009a)). A large proportion of this variation is attributable to differences in the type and number of anatomical locations examined, differences in the specific manifestation of the disease considered and to breed differences (Philipsson et al 1993;Pieramati et al 2003;van Grevenhof et al 2009a;Wittwer et al 2006). A recent prevalence estimate of 25% for the Thoroughbred (Lepeule et al 2009) appears 5 typical.…”

Section: Introductionmentioning

confidence: 99%

“…The disease is considered multifactorial in origin with at least some evidence of both environmental factors, for example nutrition, and physiological factors, such as growth and body size, endocrine factors and conformation, which may themselves be mediated through genetics, playing a role in the condition (Lepeule et al 2009;McIlwraith 2004;van Weeren et al 1999). Low to moderate estimates of heritability for OC across a range of breeds and disease manifestations (Philipsson et al 1993;Pieramati et al 2003;Schougaard et al 1990;van Grevenhof et al 2009b;Wittwer et al 2007a) together with between breed differences in prevalence (Lepeule et al 2009) indicate that genetic variability exists in disease susceptibility. Typical values for OC scored as a single binary trait (all joints combined) are 0.10 to 0.20 (Pieramati et al 2003;Wittwer et al 2007a) but heritability estimates of up to 0.5 have been reported for individual joints (Grøndahl and Dolvik 1993).…”

Section: Introductionmentioning

confidence: 99%

“…Low to moderate estimates of heritability for OC across a range of breeds and disease manifestations (Philipsson et al 1993;Pieramati et al 2003;Schougaard et al 1990;van Grevenhof et al 2009b;Wittwer et al 2007a) together with between breed differences in prevalence (Lepeule et al 2009) indicate that genetic variability exists in disease susceptibility. Typical values for OC scored as a single binary trait (all joints combined) are 0.10 to 0.20 (Pieramati et al 2003;Wittwer et al 2007a) but heritability estimates of up to 0.5 have been reported for individual joints (Grøndahl and Dolvik 1993).…”

Section: Introductionmentioning

confidence: 99%

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A genome-wide association study of osteochondritis dissecans in the Thoroughbred

et al. 2011

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“…In order to assess the impact of GS on practical situations, all scenarios were investigated for a lowly heritable, functional trait and a trait of high heritability. As an example for a lowly heritable trait, susceptibility to osteochondrosis (OC), with a heritability of 0.15 (Pieramati et al, 2003;Schober, 2003), was chosen. OC can cause disorders of chondral growth.…”

Section: Methodsmentioning

confidence: 99%

Integration of genomic information into sport horse breeding programs for optimization of accuracy of selection

Haberland

Borstel

Simianer

et al. 2012

Animal

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Reliable selection criteria are required for young riding horses to increase genetic gain by increasing accuracy of selection and decreasing generation intervals. In this study, selection strategies incorporating genomic breeding values (GEBVs) were evaluated. Relevant stages of selection in sport horse breeding programs were analyzed by applying selection index theory. Results in terms of accuracies of indices (r TI ) and relative selection response indicated that information on single nucleotide polymorphism (SNP) genotypes considerably increases the accuracy of breeding values estimated for young horses without own or progeny performance. In a first scenario, the correlation between the breeding value estimated from the SNP genotype and the true breeding value (5 accuracy of GEBV) was fixed to a relatively low value of r mg 5 0.5. For a low heritability trait (h 2 5 0.15), and an index for a young horse based only on information from both parents, additional genomic information doubles r TI from 0.27 to 0.54. Including the conventional information source 'own performance' into the before mentioned index, additional SNP information increases r TI by 40%. Thus, particularly with regard to traits of low heritability, genomic information can provide a tool for well-founded selection decisions early in life. In a further approach, different sources of breeding values (e.g. GEBV and estimated breeding values (EBVs) from different countries) were combined into an overall index when altering accuracies of EBVs and correlations between traits. In summary, we showed that genomic selection strategies have the potential to contribute to a substantial reduction in generation intervals in horse breeding programs.Keywords: accuracy of selection, breeding strategies, generation interval, genomic selection, sport horse ImplicationsThe availability of genomic information demands proper assessment of its impact on practical horse breeding programs. Accuracies of conventional breeding values do not increase significantly until a stallion is aged 8 to 12 years and his progeny enters competition. We showed that additional genomic information considerably increases the accuracy of breeding values estimated for foals, young horses without own performance, and horses without progeny performance. Therefore, genomic selection (GS) enables selection at an earlier stage, shortening generation intervals and opening room for increased genetic progress. Our results indicate that horse breeding organizations could likely benefit from the application of GS.

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Heritability estimation of osteochondrosis dissecans in Maremmano horses

Cited by 38 publications

References 14 publications

Refinement of a quantitative gene locus on equine chromosome 16 responsible for osteochondrosis in Hanoverian warmblood horses

Refinement of a quantitative gene locus on equine chromosome 16 responsible for osteochondrosis in Hanoverian warmblood horses

A genome-wide association study of osteochondritis dissecans in the Thoroughbred

Integration of genomic information into sport horse breeding programs for optimization of accuracy of selection

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