Genome-wide prediction of breeding values and mapping of quantitative trait loci in stratified and admixed populations

Toosi, Ali

doi:10.31274/etd-180810-2228

Cited by 1 publication

(2 citation statements)

References 163 publications

(359 reference statements)

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“…A genome‐wide association analysis was conducted using the Bayesian genomic prediction statistical models, which analyze all SNPs simultaneously but, other than trial, did not explicitly include additional factors to account for population structure. However, our recent research (ShaarbafToosi ) has demonstrated that these models implicitly account for population structure and that not fitting population structure explicitly does not lead to an excess of false positives in these models. One reason for this is that any SNPs that differ in allele frequencies between subpopulations can capture the effects of population structure, and thus, any effects of population structure are spread out across many SNPs across the genome.…”

Section: Discussionmentioning

confidence: 99%

“…With over 2500 1‐Mb windows, this is expected to increase the variance associated with each window only by a fraction of 1/2500 of the variance contributed by population structure, which is expected to be minimal. Furthermore, if differences due to population structure contain genetic information, allowing the SNPs to capture these effects actually increases the power to detect QTL (ShaarbafToosi ).…”

Section: Discussionmentioning

confidence: 99%

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Validation and further characterization of a major quantitative trait locus associated with host response to experimental infection with porcine reproductive and respiratory syndrome virus

et al. 2013

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Infectious diseases are costly to the swine industry; porcine reproductive and respiratory syndrome (PRRS) is the most devastating. In earlier work, a quantitative trait locus associated with resistance/susceptibility to PRRS virus was identified on Sus scrofa chromosome 4 using approximately 560 experimentally infected animals from a commercial cross. The favorable genotype was associated with decreased virus load and increased weight gain (WG). The objective here was to validate and further characterize the association of the chromosome 4 region with PRRS resistance using data from two unrelated commercial crossbred populations. The validation populations consisted of two trials each of approximately 200 pigs sourced from different breeding companies that were infected with PRRS virus and followed for 42 days post-infection. Across all five trials, heritability estimates were 0.39 and 0.34 for viral load (VL; area under the curve of logtransformed viremia from 0 to 21 days post-infection) and WG to 42 days post-infection respectively. Effect estimates of SNP WUR10000125 in the chromosome 4 region were in the same directions and of similar magnitudes in the two new trials as had been observed in the first three trials. Across all five trials, the 1-Mb region on chromosome 4 explained 15 percent of genetic variance for VL and 11 percent for WG. The effect of the favorable minor allele at SNP WUR10000125 was dominant. Ordered genotypes for SNP WUR10000125 showed that the effect was present irrespective of whether the favorable allele was paternally or maternally inherited. These results demonstrate that selection for host response to PRRS virus infection could reduce the economic impact of PRRS. SummaryInfectious diseases are costly to the swine industry; porcine reproductive and respiratory syndrome (PRRS) is the most devastating. In earlier work, a quantitative trait locus associated with resistance/susceptibility to PRRS virus was identified on Sus scrofa chromosome 4 using approximately 560 experimentally infected animals from a commercial cross. The favorable genotype was associated with decreased virus load and increased weight gain (WG). The objective here was to validate and further characterize the association of the chromosome 4 region with PRRS resistance using data from two unrelated commercial crossbred populations. The validation populations consisted of two trials each of approximately 200 pigs sourced from different breeding companies that were infected with PRRS virus and followed for 42 days post-infection. Across all five trials, heritability estimates were 0.39 and 0.34 for viral load (VL; area under the curve of logtransformed viremia from 0 to 21 days post-infection) and WG to 42 days post-infection respectively. Effect estimates of SNP WUR10000125 in the chromosome 4 region were in the same directions and of similar magnitudes in the two new trials as had been observed in the first three trials. Across all five trials, the 1-Mb region on chromosome 4 explained 15 percent of genetic...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%