[Abstract]: Crown rot (causal organism: Fusarium pseudograminearum) is a significantdisease affecting wheat in Australia. Although first reported over 60 years ago, the disease has become more prevalent in recent years due to the adoption ofminimum tillage and stubble retention practices. Breeding for resistance to crown rot is difficult - phenotypic selection, which is usually done at harvest, istime-consuming, expensive, and subject to between year variability due to sensitivity to environmental conditions. For these reasons, the coupling ofmolecular techniques with conventional plant breeding (marker-assisted selection) has the potential to more rapidly and reliably identify genomic regionsthat contribute to resistance. The objective of this study was to identify, validate,and pyramid quantitative trait loci (QTL) for resistance to crown rot present in aW21MMT70 x Mendos doubled haploid wheat population.Replicated seedling trials were conducted in 2001, 2003, and 2005. In eachseedling trial, W21MMT70 displayed partial resistance to crown rot whereasMendos seedlings were susceptible. A bulked segregant analysis (BSA), using390 simple sequence repeat (SSR) markers chosen for their coverage of thewheat genome, was initially conducted based upon the 2001 seedling trial data inan attempt to rapidly identify genomic regions associated to resistance. The BSAdid not reveal any markers associated with resistance to crown rot. As a result, afull mapping study was conducted. One hundred and twenty eight (128) SSRmarkers were mapped across the population to produce a framework map.Previously screened AFLP markers were added to the map. Composite intervalmapping revealed eight QTL associated with resistance. Of these, three (locatedon chromosomes 2B, 2D, and 5D) were consistently detected in each of the threeseedling trials. Two QTL (on chromosomes 1A and 3B) were detected in two ofthe three trials. The 2D, 3B, and 5D QTL were inherited from W21MMT70,whereas the 1A and 2B QTL were inherited from Mendos.Two software programs were used to identify epistatic interactions betweenQTL. While the results of the two programs differed markedly, both programsdetected a highly significant interaction between the W21MMT70 inherited 5DQTL and a locus on chromosome 2D inherited from Mendos. The overall effectof the epistatic interactions was not as great as the additive effects of nonepistaticQTL. Nonetheless, the presence of epistasis may indicate that,particularly in the case of 5D, the effect of this QTL may be dependent on thebackground into which it is introgressed.Validation of three W21MMT70-inherited QTL (on chromosomes 2D, 3B, and5D) was conducted on three F2 populations with W21MMT70 as one of theparents. While the 5D QTL was validated in two of the three crosses, neither the2D nor the 3B QTL were detected in any of the F2 validation populations. It islikely that the size of the F2 populations (the largest composed of 94 individuals),in conjunction with the variability that is inherent when screening for resistanceto crown rot, precluded validation of these regions. Validation of the 2BMendos-inherited QTL was conducted on a Sunco x Batavia doubled haploidpopulation because Sunco possesses the same Triticum timopheevi 2B introgression that is present in Mendos. This validated QTL (designatedQ.CR..usq-2B2) explained 11 % of the phenotypic variance in the Sunco xBatavia population.To assess the effectiveness of pyramiding QTL for resistance to crown rot, a 2-49x W21MMT70 population was examined. A number of lines of this populationperformed significantly better than each of the parents in the replicated seedlingtrial that was conducted. Four QTL, located on chromosomes 1A, 1D, 2D, and3B, were detected. The 1A and 1D QTL were inherited from 2-49 whereas the2D and 3B QTL were inherited from W21MMT70. The 1A QTL from 2-49 hasnot been previously validated, and this QTL has been designated QCr.usq-1A1.The 3B QTL (designated QCr.usq-3B1) had the highest effect (LRS 42.1;explaining 21.0 % of the phenotypic variance) in the 2-49 x W21MMT70population. The 2D QTL (QCr.usq-2D1) was shown to have a minor effect. The5D QTL that was inherited from W21MMT70 in the W21MMT70 x Mendospopulation was not detected in the 2-49 x W21MMT70 population. A number ofpossible explanations for the inability to detect this QTL in the 2-49 xW21MMT70 population are discussed.
| Identifer | oai:union.ndltd.org:ADTP/220924 |
| Date | January 2007 |
| Creators | Bovill, William D. |
| Publisher | University of Southern Queensland, Faculty of Sciences |
| Source Sets | Australiasian Digital Theses Program |
| Language | English |
| Detected Language | English |
| Rights | http://www.usq.edu.au/eprints/terms_conditions.htm, (c) Copyright 2007 William D. Bovill |
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