The advantages of open-pollinated (OP) family testing over controlled crossing (i.e., structured pedigree) are the potential to screen and rank a large number of parents and offspring with minimal cost and efforts; however, the method produces inflated genetic parameters as the actual sibling relatedness within OP families rarely meets the half-sib relatedness assumption. Here, we demonstrate the unsurpassed utility of OP testing after shifting the analytical mode from pedigree- (ABLUP) to genomic-based (GBLUP) relationship using phenotypic tree height (HT) and wood density (WD) and genotypic (30k SNPs) data for 1126 38-year-old Interior spruce ( (Moench) Voss x Parry ex Engelm.) trees, representing 25 OP families, growing on three sites in Interior British Columbia, Canada. The use of the genomic realized relationship permitted genetic variance decomposition to additive, dominance, and epistatic genetic variances, and their interactions with the environment, producing more accurate narrow-sense heritability and breeding value estimates as compared to the pedigree-based counterpart. The impact of retaining (random folding) vs. removing (family folding) genetic similarity between the training and validation populations on the predictive accuracy of genomic selection was illustrated and highlighted the former caveats and latter advantages. Moreover, GBLUP models allowed breeding value prediction for individuals from families that were not included in the developed models, which was not possible with the ABLUP. Response to selection differences between the ABLUP and GBLUP models indicated the presence of systematic genetic gain overestimation of 35 and 63% for HT and WD, respectively, mainly caused by the inflated estimates of additive genetic variance and individuals' breeding values given by the ABLUP models. Extending the OP genomic-based models from single to multisite made the analysis applicable to existing OP testing programs.
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http://dx.doi.org/10.1007/s11032-018-0784-3 | DOI Listing |
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Caretaker Medical, 941 Glenwood Station Ln #301, Charlottesville, VA 22901, United States of America.
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Department of Psychology, Michigan State University, USA.
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From the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
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January 2025
GenPhySE, Université de Toulouse, INRAE, ENVT, 31326, Castanet-Tolosan, France.
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View Article and Find Full Text PDFPLoS Genet
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Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki, Helsinki, Finland.
Recent statistical approaches have shown that the set of all available genetic variants explains considerably more phenotypic variance of complex traits and diseases than the individual variants that are robustly associated with these phenotypes. However, rapidly increasing sample sizes constantly improve detection and prioritization of individual variants driving the associations between genomic regions and phenotypes. Therefore, it is useful to routinely estimate how much phenotypic variance the detected variants explain for each region by taking into account the correlation structure of variants and the uncertainty in their causal status.
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