Genetic resistance to Fusarium head blight (FHB), caused by Fusarium graminearum, is necessary to reduce the wheat grain yield and quality losses caused by this disease. Development of resistant cultivars has been slowed by poorly adapted and incomplete resistance sources and confounding environmental effects that make screening of germplasm difficult. DNA markers for FHB resistance QTLs have been identified and may be used to speed the introgression of resistance genes into adapted germplasm. This study was conducted to identify and map additional DNA markers linked to genes controlling FHB resistance in two spring wheat recombinant inbred populations, both segregating for genes from the widely used resistance source ’Sumai 3’. The first population was from the cross of Sumai 3/Stoa in which we previously identified five resistance QTLs. The second population was from the cross of ND2603 (Sumai 3/Wheaton) (resistant)/ Butte 86 (moderately susceptible). Both populations were evaluated for reaction to inoculation with F. graminearum in two greenhouse experiments. A combination of 521 RFLP, AFLP, and SSR markers were mapped in the Sumai 3/Stoa population and all DNA markers associated with resistance were screened on the ND2603/Butte 86 population. Two new QTL on chromosomes 3AL and 6AS wer found in the ND2603/Butte 86 population, and AFLP and SSR markers were identified that explained a greater portion of the phenotypic variation compared to the previous RFLP markers. Both of the Sumai 3-derived QTL regions (on chromosomes 3BS, and 6BS) from the Sumai 3/Stoa population were associated with FHB resistance in the ND2603/Butte 86 population. Markers in the 3BS QTL region (Qfhs.ndsu-3BS) alone explain 41.6 and 24.8% of the resistance to FHB in the Sumai 3/Stoa and ND2603/Butte 86 populations, respectively. This region contains a major QTL for resistance to FHB and should be useful in marker-assisted selection.

A major fusarium head blight (FHB) resistance gene Fhb1 (syn. Qfhs.ndsu-3BS) was fine mapped on the distal segment of chromosome 3BS of spring wheat (Triticum aestivum L.) as a Mendelian factor. FHB resistant parents, Sumai 3 and Nyubai, were used as sources of this gene. Two mapping populations were developed to facilitate segregation of Qfhs.ndsu-3BS in either a fixed resistant (Sumai 3*5/Thatcher) (S/T) or fixed susceptible (HC374/3*98B69-L47) (HC/98) genetic background (HC374 = Wuhan1/Nyubai) for Type II resistance. Type II resistance (disease spread within the spike) was phenotyped in the greenhouse using single floret injections with a mixture of macro-conidia of three virulent strains of Fusarium graminearum. Due to the limited heterogeneity in the genetic background of the crosses and based on the spread of infection, fixed recombinants in the interval between molecular markers XGWM533 and XGWM493 on 3BS could be assigned to discrete

Fusarium head blight (FHB) is a destructive disease that reduces wheat grain yield and quality. To date, the quantitative trait locus on 3BS (Fhb1) from Sumai 3 has shown the largest effect on FHB resistance. Single nucleotide polymorphism (SNP) is the most common form of genetic variation and is suitable for high-throughput marker-assisted selection (MAS). We analyzed SNPs derived from 23 wheat expressed sequence tags (ESTs) that previously mapped near Fhb1 on chromosome 3BS. Using 71 Ning 7840/Clark BC7F7 recombinant inbred lines and the single-base extension method, we mapped seven SNP markers between Xgwm533 and Xgwm493, flanking markers for Fhb1. Five of the SNPs explained 45-54% of the phenotypic variation for FHB resistance. Haplotype analysis of 63 wheat accessions from eight countries based on SNPs in EST sequences, simple sequence repeats, and sequence tagged sites in the Fhb1 region identified four major groups: (1) US-Clark, (2) Asian, (3) US-Ernie, and (4) Chinese Spring. The Asian group consisted of Chinese and Japanese accessions that carry Fhb1 and could be differentiated from other groups by marker Xsnp3BS-11. All Sumai 3-related accessions formed a subgroup within the Asian group and could be sorted out by Xsnp3BS-8. The SNP markers identified in this study should be useful for MAS of Fhb1 and fine mapping to facilitate cloning of the Fhb1 resistance gene.

采用区间作图和复合区间作图方法对重组自交系群体宁894037/Alondra、望水白/Alondra和苏麦3号/Alondra进行了抗赤霉病QTL分析，结果表明，用在田间和温室的赤霉病抗性鉴定资料，在3个赤霉病抗源宁894037、望水白和苏麦3号的3B染色体短臂上均检测到主效QTL的存在。宁894037主效QTL位于标记BARC133与Xgwm493之间的5.0 cM的区间内，最高可解释42.8%的赤霉病抗性；望水白的主效QTL位于标记BARC147与Xgwm493之间11.5 cM的区间内，最高可解释15.1%的赤霉病抗性；苏麦3号的主效QTL位于Xgwm533a与Xgwm493之间13.0 cM的区间内，最高可解释10.6%的赤霉病抗性。与赤霉病抗性主效QTL紧密连锁的标记均为SSR标记，可直接用于分子辅助育种。

通过分子标记辅助选择技术和回交育种方法，以苏麦3号为抗赤霉病基因Fhb1和Fhb2的供体亲本，以弱筋感病品种扬麦13为受体和轮回亲本，对扬麦13进行赤霉病抗性改良。利用抗性基因紧密连锁的SSR标记筛选和田间赤霉病抗性鉴定，获得8个农艺性状似轮回亲本且含有目标基因的品系。通过分子标记对其进行遗传背景分析，获得3个与轮回亲本基本相同的品系。对这3个品系和扬麦13进行赤霉病接种鉴定和主要品质指标检测与比较，最终培育出携带赤霉病抗性基因且保持轮回亲本优良农艺性状及弱筋品质的品系R扬麦13 2、R扬麦13 7和R扬麦13 8，赤霉病病小穗率降低了78.82%~84.58%，产量提高了17.24%~26.72%，完全可以替代当前生产上高感赤霉病的扬麦13品种进行推广应用。这表明利用与抗性基因紧密连锁的分子标记辅助育种是一种有效的途径，可以实现小麦赤霉病抗性改良的目标。

Fusarium head blight (FHB), which is mainly caused by Fusarium graminearum, is a destructive wheat disease that threatens global wheat production. Fhb1, a quantitative trait locus discovered in Chinese germplasm, provides the most stable and the largest effect on FHB resistance in wheat. Here we show that TaHRC, a gene that encodes a putative histidine-rich calcium-binding protein, is the key determinant of Fhb1-mediated resistance to FHB. We demonstrate that TaHRC encodes a nuclear protein conferring FHB susceptibility and that a deletion spanning the start codon of this gene results in FHB resistance. Identical sequences of the TaHRC-R allele in diverse accessions indicate that Fhb1 had a single origin, and phylogenetic and haplotype analyses suggest that the TaHRC-R allele most likely originated from a line carrying the Dahongpao haplotype. This discovery opens a new avenue to improve FHB resistance in wheat, and possibly in other cereal crops, by manipulating TaHRC sequence through bioengineering approaches.

为给小麦抗赤霉病遗传改良提供参考，利用苏麦3号及5个当地推广小麦品种为亲本，按Griffing双列杂交法Ⅱ配制15个杂交组合，以赤霉病病小穗率为抗性指标，研究了小麦赤霉病抗性的遗传。结果表明，在6个小麦品种中，苏麦3号和扬麦9号赤霉病抗性的一般配合力最好，能极显著地提高杂种后代的赤霉病抗性。小麦赤霉病抗性的遗传符合加性 显性模型，同时受加性和显性效应的作用，且加性效应更重要，显性程度为部分显性。控制赤霉病遗传的增效等位基因为显性，增减效等位基因频率在亲本中的分配存在显著差异。苏麦3号具有最多的控制赤霉病抗性遗传的显性基因，而宁麦8号则具有控制赤霉病抗性遗传最多的隐性基因。小麦赤霉病抗性可能受2~3对主效基因的控制，狭义遗传力较高，早代选择有效。论文最后还就小麦抗赤霉病育种进行了探讨。

赤霉病（Fusarium head blight,FHB）是小麦最主要的病害之一,严重影响小麦生产安全和食品安全,研究小麦赤霉病抗性机理对于解决小麦赤霉病这一世界性难题具有重要意义。根据对赤霉病的抗性表现形式,将小麦赤霉病抗性分为五个大类,分别为抗侵入（Type I）、抗扩展（Type II）、籽粒抗感染（Type III）、耐病性（Type Ⅳ）和抗毒素积累（Type V）。小麦赤霉病的抗性机理可以分为形态机制和生理机制,形态抗性机制是被动的,株高、抽穗期、花期长短、花药挤出程度、有芒无芒、穗长、穗密度、颖壳张开程度和穗部蜡质程度等形态特征均可能与赤霉病抗侵染特性有关。细胞学研究表明,病原菌侵染后抗病品种可迅速从细胞结构和生理生化方面产生防卫反应,通过乳突、胞壁沉积物的形成以及木质素、硫堇、富含羟脯氨酸糖蛋白和水解酶类等的增长来协同抵御病菌在体内的扩展。在植物复杂的信号途径中,水杨酸（SA）、茉莉酸（JA）和乙烯（ET）3种信号途径在植物抵御病原菌入侵中的作用最为重要,SA和ET信号途径对小麦赤霉病抗性方面的作用目前还存在一定争议,而JA信号途径在小麦赤霉病抗性中积极作用已经被多数研究者所证实。迄今为止,人类定位了200个以上不同类型的抗赤霉病QTL位点,这些位点分布于所有的小麦染色体,其中的22个QTL位点被不同的作图群体所定位,包括2个定位在3BS和6BS染色体上稳定的抗扩展位点Fhb1和Fhb2,以及2个定位在4B和5A染色体上的抗侵染位点Fhb4和Fhb5。在受到病原菌侵染后,植物会产生一系列复杂的信号途径激活应答反应,诱导抗病相关基因的表达,进而引起蛋白以及代谢水平的变化,抵御病原菌的侵袭,研究表明,病程相关蛋白基因、抗菌肽基因、转录因子基因、脱毒相关蛋白基因以及其他赤霉病抗性相关基因均参与了小麦赤霉病抗性提高的过程。随着生物工程技术和生物信息技术的迅猛发展,将来可利用图位克隆技术分离抗赤霉病主效基因,并在全基因组关联分析和各种组学技术的基础上,从全基因组和基因调控网络水平上研究小麦赤霉病抗性机理,以期在更深层次上理解小麦赤霉病的抗性机理。