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望水白×南大2419群体抗赤霉病QTL的初步分析
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摘要
由赤霉菌引起的小麦赤霉病是小麦生产的主要病害之一。培育抗病品种是防治赤霉病最安全、有效的措施。然而,抗源匮乏和抗性遗传机制不清严重地限制了小麦抗赤霉病育种的进展。因此,发掘新的抗病基因,并对其进行基因定位是目前小麦赤霉病研究的主要内容之一。分子标记技术的发展和QTL作图方法的不断完善,为深入开展赤霉病抗性遗传分析提供了基础。
     望水白是我国江苏的地方品种,为少数几个优异小麦赤霉病抗源之一。开展对望水白抗赤霉病QTL的研究,有助于阐明赤霉病抗性遗传机制,为人们通过育种方法累加不同来源的抗性基因提供理论基础。
     本研究构建了望水白×南大2419的F_6代重组自交系群体,并分别在温室和田间对其进行了赤霉病抗性鉴定。利用RAPD和SSR分子标记对该群体株系进行了基因型分析,获得了10个与赤霉病抗性显著相关的标记位点(p<0.05),它们分别是Xnau23、Xnau16.3、Xnau16.2、Xnau22、Xnau11.2、Xnau11.1、Xnaul、Xnau14.1、Xnau6.1和Xnau27。其中,分别与病小穗数、病节数和病节长度显著相关的位点有6个、10个和8个。可能由于性状间的相关性,有些标记位点与一个以上的性状相关。Xnau16.3、Xnau16.2、Xnau22和Xnau11.1与病节数和病节长度的相关性在本研究两个试验(温室和田间)间有很好的一致性,以Xnau16.3和Xnau22对病节数和病节长度的效应较大。连锁分析表明,上述与赤霉病
    
    抗性相关的位点分别位于染色体ZB、3A、3B和SB上。
     通过区间作图分析,一个QTL被定位于xnau23一Xnau22之间,另一
    个被定位于xnaul了.了一xnau24之间,二者的抗性等位基因均来源于抗病
    亲本望水白。位于Xnau23一Xnau22之间的效应较大,分别解释了温室试
    验中20.1%的病节数变异和15.9%的病节长度变异,及田间试验中n.2%
    的病节数变异和11.6%的病节长度变异。还有一个QTL被定位于xnau了一
    xnau14.了之间,它解释了田间试验中9.0%的病节数变异。该QTL的抗
    性等位基因来源于感病亲本南大2419。
Fusarium head blight (FHB), caused by Fusarium graminearum Schwabe (telomorph: Gibberella zeae), is a major disease of wheat. Outbreak of FHB can result in devastating economic losses to wheat production, since it not only lowers the yield but also deteriorates the quality of wheat grains. Deployment of scab-resistant varieties is the most economical measure in controlling this disease. However, the paucity of germplasms and lack of knowledge about the resistance genetics have greatly limited the progress in scab resistance breeding. To identify genes for scab resistance, a population of F6 recombinant inbred lines (RILs) from a cross 'Wangshuibai'(resistant) x 'Nanda 2419'(susceptible) was produced. The population was evaluated in a greenhouse and a field for FHB resistance through single floret inoculation of the conidia at flowering stage. Mist system was used to maintain the moisture suitable for disease development. Fifteen days after the inoculation, data were
    
    
    collected for number of diseased spikelets, number of diseased internodes and length of diseased rachis. SSR and RAPD markers were screened for polymorphisms between the parents and between the resistant and susceptible pools. The polymorphic markers were applied in genotyping of the populations. Using one-way ANOVA and regression analysis, ten markers were found to be significantly associated with FHB resistance (p<0.05), including 6 with the number of diseased spikes, 10 with the number of diseased internodes and 8 with the length of diseased rachis. Because of the trait correlation, some of the markers were shared among the three traits. Among the ten markers, four which showed association with the number of diseased internodes and the length of diseased rachis were consentaneous in the greenhouse and field test. These ten markers were mapped to chromosomes 2B, 3A, 3B and 5B, respectively.
    By interval analysis, three intervals showed significant association with FHB resistance. Two of them were located between Xnau23 - Xnau22 and between Xnaull. 1 - Xnau24. The resistance alleles of both loci derived from the resistant parent 'Wangshuibai'. The third interval was located between SSR1021 and Xnaul4.1. The resistance allele of this QTL derived from the susceptible parent 'Nanda 2419'. The one between Xnau23 - Xnau22 has the largest effect, explaining 20.1% and 15.9% of the phenotypic variance for the
    
    number of diseased internodes and the length of diseased rachis respectively in the greenhouse test, and 11.2% and 11.6% of the phenotypic variance respectively for these two traits in the field test. The identification of QTLs for scab resistance paves the way for discovery of scab resistance genes and marker-assisted selection of scab resistance.
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