水稻稻瘟病抗性基因定位、克隆及应用

稻瘟病是水稻生产中最严重的病害之一,严重影响水稻的产量和品质,由于稻瘟菌小种的变异快,垂直抗性基因难以持续控制稻瘟病的危害,因此,定位和克隆广谱持久的稻瘟病抗性基因,揭示其作用的分子机理,结合分子育种技术培育高产优质多抗的水稻新品种将是今后解决稻瘟病抗性育种最有效的途径.本文综述了水稻和稻瘟病菌之间的互作,稻瘟病抗性的分子机制,稻瘟病抗性基因定位,目前已经定位了73个稻瘟病质量抗性基因,其中9个稻瘟病抗性基因已经被克隆并进行了深入的研究,此外定位了至少11个QTL以及稻瘟病抗性基因克隆和功能分析,及其在水稻抗病育种中的应用.     

水稻-病原菌互作途径研究进展

水稻稻瘟病和白叶枯病分别由真菌病原菌Magnaporthe oryzae (M. oryzae)和细菌病原菌 Xanthomonas oryzae pv. oryzae (Xoo)引起,是造成世界范围内水稻减产的主要病因,水稻-稻瘟病菌及水稻-白叶枯病原菌互作已成为研究植物-病原菌互作的模式系统。本文归纳了目前已克隆的抗稻瘟病及白叶枯病基因与其分子结构和功能,概括了近年来鉴定的一些病原菌相关分子(Pathogen-associated molecular patterns,PAMPs)及稻瘟病菌和白叶枯菌分泌的效应蛋白,并总结了针对稻瘟病菌和白叶枯菌介导的病原物分子诱导的抗病反应(PAMP-triggered immunity,PTI)和效应蛋白诱导的抗病性(Effector-triggered immunity,ETI)及其信号传导途径的研究成果,指出效应蛋白-抗病蛋白间互作将为探索植物-病原菌间互作提供新的分子基础,并为水稻抗病育种实践提供借鉴与指导。     

水稻-病原菌互作途径研究进展

水稻稻瘟病和白叶枯病分别由真菌病原菌Magnaporthe oryzae (M. oryzae)和细菌病原菌 Xanthomonas oryzae pv. oryzae (Xoo)引起,是造成世界范围内水稻减产的主要病因,水稻-稻瘟病菌及水稻-白叶枯病原菌互作已成为研究植物-病原菌互作的模式系统。本文归纳了目前已克隆的抗稻瘟病及白叶枯病基因与其分子结构和功能,概括了近年来鉴定的一些病原菌相关分子(Pathogen-associated molecular patterns,PAMPs)及稻瘟病菌和白叶枯菌分泌的效应蛋白,并总结了针对稻瘟病菌和白叶枯菌介导的病原物分子诱导的抗病反应(PAMP-triggered immunity,PTI)和效应蛋白诱导的抗病性(Effector-triggered immunity,ETI)及其信号传导途径的研究成果,指出效应蛋白-抗病蛋白间互作将为探索植物-病原菌间互作提供新的分子基础,并为水稻抗病育种实践提供借鉴与指导。     

利用分子标记和接种鉴定分析美国水稻育种亲本的稻瘟病抗性

稻瘟病是由真菌Magnaporthe oryzae引起的,水稻与稻瘟病菌的互作符合经典的“基因对基因”学说,抗稻瘟病基因Pi-ta可有效防治携带A VR-Pita1稻瘟菌的侵染.本研究利用位于Pi-ta基因前端的显性 .分子标记YLI53/YL153和位于中间区域的显性分子标记YL155/YL87对39份来自美国的水稻...     

吉林省水稻品种对稻瘟病的抗性分析

选用22个稻瘟菌鉴别菌株,采用离体叶片接种法对吉林省全部水稻主栽品种及育种材料(98个)的抗瘟性进行了鉴定.结果显示,吉林省主栽水稻品种对稻瘟病的抗性较弱,高达98%的供试品种均可以被稻瘟菌不同程度地侵染;本研究筛选到3个品种:超级稻2号、吉粳801、吉粳806,具有极高的抗瘟性,为将来克隆新的抗瘟基因及培育新的抗瘟品...     

利用基因沉默技术创造抗稻瘟病水稻资源

水稻稻瘟病是最具毁灭性的病害之一,严重地影响水稻的高产和稳产。在病原菌侵染水稻时,附着胞的形成对稻瘟病菌的致病性起着关键作用。研究证实一种P型ATP酶（ P-ATPase）参与了附着胞的形成。在病原菌与寄主的互作过程中,寄主的一些小分子物质可以进入病原菌中,达到抗病原菌侵染的目的。以稻瘟菌致病关键的P-AT-Pase基因MgAPT2第一外显子上特异性好的232 bp的区域作为干扰片段,正反向插入干扰载体中,通过农杆菌介导,转化到感稻瘟病水稻品种日本晴中,通过苗期稻瘟病接种鉴定和MgAPT2基因的表达检测,结果表明：转基因植株稻瘟病抗性得到增强且稻瘟病菌MgAPT2基因的表达量下降,为水稻抗稻瘟病种质资源的创新提供了新思路。     

王国梁研究团队合作在水稻-稻瘟菌互作研究方面取得重要进展

<正>近日,病原学领域国际权威期刊PloS Pathogens发表了中国农业科学院植物保护研究所王国梁研究员团队与中国农业大学王毅教授团队合作完成的题为"The fungal pathogen Magnaportheoryzae suppresses innate immunity by modulating a host potassium channel"的研究论文。该研究通过分析鉴定稻瘟菌效应蛋白在水稻中靶标蛋白,揭示了稻瘟菌侵染的新机制。由稻瘟菌侵染引起的稻瘟病俗称水稻"癌症",往往造成水稻严重减产。深入研究水稻-稻瘟菌互作机制,对提     

稻瘟菌效应蛋白研究进展

稻瘟菌是一种在世界范围内严重危害水稻生产的真菌病原。在稻瘟菌与水稻互作过程中,稻瘟菌效应蛋白起着至关重要的作用。针对效应蛋白功能及其作用机理的研究有助于阐明稻瘟菌与水稻互作分子机制,并为未来水稻抗病改良提供新的理论策略。本文综述了稻瘟菌效应蛋白研究的进展,并重点针对基因克隆、蛋白转运以及功能机制等方面介绍了稻瘟菌Avr蛋白研究的最新发现,同时对未来值得重点关注的研究方向进行了探讨。     

水稻材料IR65482抗稻瘟病基因鉴定与定位

水稻材料IR65482对不同地区的稻瘟菌小种具有广谱抗性,已知其第6号染色体上具有一个抗稻瘟病病基因Pi40(t)。本研究应用极端分离混合池重测序策略,对IR65482抗稻瘟病基因进行鉴定,并在其第11号染色体上鉴定到另一个抗稻瘟病基因。进一步利用IR65482与日本晴配置的F2群体进行基因定位,将IR65482抗稻瘟病基因定位在水稻第11染色体末端InDel标记OSL3-2和OSL3-5之间约425 kb的区间。本研究结果对利用IR65482开展水稻抗稻瘟病育种具有指导意义,也为后续克隆IR65482的抗病基因提供了理论依据。     

稻瘟病苗瘟叶瘟和穗颈瘟的相关性分析

采用温室人工接菌法探讨水稻稻瘟病苗瘟、叶瘟和穗颈瘟的相关性,研究结果表明,稻瘟病苗瘟、叶瘟和穗颈瘟三者之间存在着一定的正相关性,相关程度因水稻品种、稻瘟病菌生理小种的不同而有所差异。此外,对水稻品种温室苗瘟抗性率与田间叶瘟抗性率、穗颈瘟抗性率之间的相关性进行研究,结果表明温室苗瘟抗性率与自然病圃叶瘟抗性率表现正相关关系(r=0.5435),温室苗瘟抗性率与自然病圃穗颈瘟抗性率表现极显著正相关关系(r=0.7583**,p<0.01),自然病圃叶瘟抗性率与穗颈瘟抗性率呈显著正相关关系(r=0.6322*,p<0.05)。因此,认为利用可控温室代替田间进行水稻品种稻瘟病抗性鉴定是可行的,而且根据苗瘟、叶瘟的抗性鉴定结果推测穗颈瘟的抗性基本上也是可行的。     

番茄叶霉菌无毒基因的研究进展

无毒基因是病原物遗传因子,其编码的产物激发病原物与植物特异性相互作用。病原物无毒基因与植物抗病基因产物间直接或间接相互作用导致产生的基因对基因抗性是植物抗病性的重要形式。番茄与叶霉病之间的特异互作被认为是遵循Flor的“基因对基因”假说的典型体系。绝大多数已克隆的无毒基因之间,及其与已知蛋白之间,均无显著的序列同源性。无毒基因具有双重功能：在含瓦补抗性基因植物中表现无毒效应,而在不含互补抗性基因植物中显示毒性效应。本文综述了番茄叶霉菌无毒基因的多样性、意义、结构及其功能等等,了解病原菌无毒基因的结构及功能,有助于了解病原物与植物的识别机制,对认识植物的抗病性,特别是非寄主植物对病原菌的广谱抗病性也具有重要意义。     

A Compendium on Host Genes in Flax Conferring Resistance to Flax Rust

A list with information about named host genes controlling resistance to rust in both cultivated and wild flax has been compiled. These will be useful for genetic, physiological and biochemical research as well as breeding for resistance. Information regarding mutation, temperature sensitivity and the effect of inhibitor/avirulence gene interaction on expression of certain host genes is included.     

水稻白叶枯病抗性研究进展

白叶枯病是世界水稻重要病害之一,且已成为研究植物和病原菌互作的模式,对该病的研究对其它病害有借鉴意义。目前已鉴定出29个抗白叶枯病基因,其中17个基因被定位到染色体上,4个基因已被克隆,在这些工作的基础上,已通过分子标记辅助选择和转基因方法育成了一些抗病新品系,展示了水稻抗白叶枯病分子育种的广阔前景。     

Counteracting virulence mechanisms of grain legume pathogens

Summary Grain legumes, in common with all other plants, are subject to biotic constraints of which pathogens form an important group. They are variable in type, number, space and time and, most insidiously, in genetic constitution. Consequently, resistance in the plant to a given pathogen may be quickly nullified by genetic alteration of the pathogen, particularly where this is conferred by a single resistance gene. The products of such resistance genes usually recognise, directly or indirectly, a component of the pathogen, which is encoded by a corresponding avirulence gene. Thus resistance and avirulence genes are specific and complementary and the arrangement is referred to as a gene-for-gene relationship. It follows that alteration of the avirulence gene of the pathogen to give a product that is no longer recognised by the product of the resistance gene of the plant gives rise to a susceptible reaction. A possible solution to this problem is to pyramid several resistance genes, a procedure now facilitated by the techniques of genetic modification. In other interactions genes that reduce susceptibility rather than confer complete resistance have been found and in some cases the loci (quantitative trait loci) responsible have been mapped to specific regions of particular chromosomes. The mechanisms by which these genes limit the virulence of the pathogen are generally unknown. However, by gaining an understanding of the fundamental properties of a pathogen that are necessary for pathogenicity or virulence it may be possible to counteract them. Candidates for such properties are toxins, enzymes and mechanisms that interfere with constitutive or active defence of the plant. Reciprocally, understanding the properties of the plant that confer susceptibility may allow selection of germplasm that lacks such properties. Among the candidates here are germination stimulants of pathogen propagules and signals that promote the formation of infection structures.     

稻瘟病菌杂交后代致病性遗传分析

为明确稻瘟病菌杂交后代对水稻致病性的遗传规律,以亲本菌株HLJ6122和KA3杂交产生的后代群体为试验材料,将其接种于14个单基因系抗性水稻品种,对杂交后代进行毒性差异分析。结果表明,64个杂交后代菌株呈现显著的毒性分离,共出现53种毒性类型,无毒性/毒性分别表现为1∶1、1∶3、3∶1、15∶1。菌株KA3分别对IRBLi-F5、IRBLta-K1、IRBL12-M、IRBLta2-Pi持有1个无毒基因;对品种IRBLa-A、IRBLzt-T、IRBL7-W、IRBLkm-Ts、IRBL20-IR24持有2个无毒基因。64个后代菌株对品种IRBLk-Ka、IRBLz-Fu、IRBL19-M、IRBLb-B、IRBLkp-K60无毒性/毒性也符合1∶3,但2个亲本菌株HLJ6122和KA3对供试水稻品种致病性相同,因此难以判断无毒基因的来源。     

Small differential interactions for partial resistance in rice cultivars to virulent isolates of the blast pathogen

Summary Six rice genotypes, differing in partial resistance, were exposed to three isolates of the blast pathogen. Of the variance due to host and pathogen genotypes, 39% was due to host genotype effects, 60% was due to isolate effects, and only 1% was due to host genotype × isolate interactions. Although small, this interaction variance was highly significant and mainly due to the IR50 × W6-1 and IR37704 × JMB8401-1 combinations. Although behaving largely as race-non-specific (large main effects only), the partial resistance cannot be classified as race-non-specific. The results suggest that minor genes for partial resistance operate in a gene for gene relationship with minor genes in the pathogen.     

The integrated concept of disease resistance: A new view including horizontal and vertical resistance in plants

Summary Horizontal, uniform, race-non-specific or stable resistance can be discerned according to Van der Plank, from vertical, differential, race-specific or unstable resistance by a test in which a number of host genotypes (cultivars or clones) are tested against a number of pathogen genetypes traces of isolatest. If the total non-environmental variance in levels of resistance is due to main effects only differences between cultivars and differences between isolates) the resistance and the pathogen many (in the broad sense) are horizontal in nature. Vertical resistance and pathogenicity are characterized by the interaction between host and pathogen showing up as a variance compenent in this test due to interaction between cultivars and isolates.A host and pathogen model was made in which resistance and pathogenicity are governed by live polygenic loci. Within the host the resistance genes show additivity. Two models were investigated in model I resistance and pathogenicity genes operate in an additive way as envisaged by Van der Plank in his horizontal resistance. Model II is characterized by a gene-for-gene action between the polygenes of the host and those of the pathogen.The cultivar isolate test in model I showed only main effect variance. Surprisingly, the variance in model II was also largely due to main effects. The contribution of the interaction to the variance uppeared so small, that it would be difficult to discern it from a normal error variance.So-called horizontal resistance can therefore be explained by a polygenic resistance, where the individual genes are vertical and operating on a gene-for-gene basis with virulence genes in the pathogen. The data reported so far support the idea that model II rather than model I is the realistic one.The two models also revealed that populations with a polygenic resistance based on the gene-for-gene action have an increased level of resistance compared with the addition model, while its stability as far as mutability of the pathogen is concerned, is higher compared to those with an additive gene action. Mathematical studies of Mode too support the gene-for-gene concept.The operation of all resistance and virulence genes in a natural population is therefore seen as one integrated system. All genes for true resistance in the host population, whether they are major or minor genes are considered to interact in a gene-for-gene way with virulence genes either major or minor, in the pathogen population.The models revealed other important aspects. Populations with a polygenic resistance based on a gene-for-gene action have an increased level of resistance compared to populations following the addition model. The stability, as far as mutability of the pathogen is concerned, is higher in the interaction model than in the addition model.The effect of a resistance gene on the level of resistance of the population consists of its effect on a single plant times its gene frequency in the population. Due to the adaptive forces in both the host and the pathogen population and the gene-for-gene nature of the gene action an equilibrium develops that allows all resistance genes to remain effective although their corresponding virulence genes are present. The frequencies of the resistance and virulence genes are such that the effective frequencies of resistance genes tend to be negatively related to the magnitude of the gene effect. This explains why major genes often occur at low frequencies, while minor genes appear to be frequent. It is in this way that the host and the pathogen, both as extremely variable and vigorous populations, can co-exist.Horizontal and vertical resistance as meant by Van der Plank therefore do not represent different kinds of resistances, they represent merely polygenic and oligogenic resistances resp. In both situations the individual host genes interact specifically with virulence genes in the pathogen. Van der Plank's test for horizontal resistance appears to be a simple and sound way to test for polygenic inheritance of resistance.The practical considerations have been discussed. The agro-ecosystems should be made as diverse as possible. Multilines, polygenic resistance, tolerance, gene deployment and other measures should be employed, if possible in combination.     

Genetic analysis of resistance/susceptibility in individual F3 families of rice against strains of Magnaporthe grisea containing different genes for avirulence

A cross was made between rice cultivars Katy and Lemont. F3 families were produced from individual F2 plants. Approximately 25 plants of each F3 family were inoculated with each of 8 different strains of Magnaporthe grisea. Each strain of the pathogen was known to have different genes for avirulence on Katy or Lemont. Each F3 family was recorded as having all plants resistant, segregating for resistance, or all plants being susceptible. The results suggest that the ‘single’ gene for resistance in Katy is a tightly linked cluster of at least seven genes. This revised version was published online in July 2006 with corrections to the Cover Date.