| Literature DB >> 26660464 |
Sen Han1, H Friedrich Utz1, Wenxin Liu2, Tobias A Schrag1, Michael Stange1,3, Tobias Würschum4, Thomas Miedaner4, Eva Bauer5, Chris-Carolin Schön5, Albrecht E Melchinger6.
Abstract
KEY MESSAGE: QTL analysis for Fusarium resistance traits with multiple connected families detected more QTL than single-family analysis. Prediction accuracy was tightly associated with the kinship of the validation and training set. ABSTRACT: QTL mapping has recently shifted from analysis of single families to multiple, connected families and several biometric models have been suggested. Using a high-density consensus map with 2472 marker loci, we performed QTL mapping with five connected bi-parental families with 639 doubled-haploid (DH) lines in maize for ear rot resistance and analyzed traits DON, Gibberella ear rot severity (GER), and days to silking (DS). Five biometric models differing in the assumption about the number and effects of alleles at QTL were compared. Model 2 to 5 performing joint analyses across all families and using linkage and/or linkage disequilibrium (LD) information identified all and even further QTL than Model 1 (single-family analyses) and generally explained a higher proportion pG of the genotypic variance for all three traits. QTL for DON and GER were mostly family specific, but several QTL for DS occurred in multiple families. Many QTL displayed large additive effects and most alleles increasing resistance originated from a resistant parent. Interactions between detected QTL and genetic background (family) occurred rarely and were comparatively small. Detailed analysis of three fully connected families yielded higher pG values for Model 3 or 4 than for Model 2 and 5, irrespective of the size NTS of the training set (TS). In conclusion, Model 3 and 4 can be recommended for QTL-based prediction with larger families. Including a sufficiently large number of full sibs in the TS helped to increase QTL-based prediction accuracy (rVS) for various scenarios differing in the composition of the TS.Entities:
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Year: 2015 PMID: 26660464 DOI: 10.1007/s00122-015-2637-3
Source DB: PubMed Journal: Theor Appl Genet ISSN: 0040-5752 Impact factor: 5.699