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1.
植物抗病基因特异性分子进化   总被引:4,自引:0,他引:4  
病原物与寄主间长期的相互选择与适应,使得植物的抗病性具有丰富的表现形式。根据基因对基因模式,植物中存在的抗病基因和病原物中具备的无毒基因的互作进化可视为连续的步步适应的相互选择的过程。随着抗病基因的分离以及抗病性分子生物学研究的不断深入,抗病基因保持对无毒基因的识别从而不断进化的分子机制逐步得到阐明。本文综述了植物与病原物相互作用过程中,植物对病原物的特异性识别,由此获得的对于该病原物的专化抗性,并且随病原物的变异而进化的分子机制方面的研究进展,主要包括:抗病基因的结构特征,无毒基因的多样性,抗病基因的基因组结构,抗病基因之间在起源和进化上的关系以及重组、复制、删除、转座子等对植物保持对不断变化的无毒基因特异性识别所起的作用等方面。  相似文献   

2.
番茄细菌性斑点病是一种严重影响番茄质量和产量的世界性细菌性病害。目前对番茄与病原菌互作的研究取得了很大进展。番茄的Pto基因是指在基因对基因学说中,对引起番茄细菌性斑点病带有AvrPto基因的致病菌Pseudomonas syingae pv. tomato(PST)起抗性作用的基因。番茄中的抗病基因Pto与病原物中的无毒基因AvrPto互作是寄主对病原物互作的典型模式系统。这一模式识别的分子机制是Pto激酶与PST的两个效应子AvrPto和AvrPtoB中的任一个发生物理互作,然后与Prf一起激活下游多重信号传导途径,进而产生抗病性反应。已基本弄清Pto抗性传导途径,但对这个途径中的许多元件的作用及环节还有待于进一步研究。  相似文献   

3.
植物病原物在侵染寄主过程中会分泌与寄主植物相互作用的蛋白,这类蛋白称为效应蛋白(效应子),这些效应蛋白在植物细胞内发挥着重要作用,从而影响植物病原物与寄主的相互作用。针对植物病原物效应子功能及其作用机理的研究将有助于更好地了解植物病原物与寄主植物相互作用的分子机制。本研究对细菌、卵菌、真菌和线虫的效应子的研究进展进行了综述,并重点阐述了这4类病原物与寄主植物相互作用的理论基础、效应子的功能机制,这些研究结果可为未来作物抗病改良和病害防控策略的制定提供参考。  相似文献   

4.
植物抗性信号分子——水杨酸研究进展   总被引:14,自引:4,他引:10  
植物在与病原物长期相互作用、共同进化过程中产生一系列防卫体系,从而有效地抑制病原物对自身的侵害。当植物受到病原物侵染时,侵染部位通常会在几小时内形成局部细胞死亡,限制病原物的增殖与扩散,称为过敏反应(Hyper sensitive Response, HR)。过敏反应几天或1周后整株植株会对其他病原物产生抗性,称为系统获得性抗性(Systemic Acquired Resistance, SAR)。SAR强调受侵染后植株获得整体抗性的能力,大量研究结果认为SAR是普遍存在的,并具有广谱性。许多研究证实,SA是SAR的重要诱导因子,也是植物受病原菌侵染后活化一系列防卫反应的信号传导途径中的重要组成成分。较为详细论述了SA在诱导植物产生抗病性过程中的作用及其研究进展,另外还对SA在其他抗性方面的作用做了简单的叙述。  相似文献   

5.
稻瘟病菌无毒基因研究进展   总被引:2,自引:0,他引:2  
水稻与稻瘟菌间存在广泛而特异的相互作用,是研究寄主与病原物互作的重要模式系统。无毒基因是病原物遗传因子,能诱发寄主植物产生抗病性,是稻瘟菌与水稻互作最重要的激发子。为寻求稻瘟病防治的新策略,本研究概述了研究稻瘟病菌无毒基因的意义,归纳了抗性基因与无毒基因互作的3种模式,总结了国内外稻瘟病菌无毒基因的克隆及功能研究,探讨了无毒基因在生产上病害流行预测中的应用,指出利用抗性基因与无毒基因的关系对稻瘟菌分类将会更为科学和实用,应进一步加快稻瘟病菌无毒基因的克隆。  相似文献   

6.
黑龙江省稻瘟病菌无毒基因的组成及其频率初析   总被引:1,自引:0,他引:1  
正稻瘟病(Magnaporthe oryzae)是世界各水稻产区广泛发生的重要真菌病害,也是黑龙江省水稻高产稳产的重要限制因子之一。培育和种植抗病品种是防治稻瘟病最经济、最有效的措施。然而,长期以来困扰育种家的问题是如何延缓抗稻瘟病水稻品种在生产中大面积种植3~5年后变成感病品种。病原菌无毒基因编码的产物能够激发病原物与植物产生特异性相互作用,水稻抗病基因产物直接或间接识别病原菌无毒基因产物时,可以诱导植株产生抗病反  相似文献   

7.
<正>植物系统获得抗病性是植物抵抗病原物侵染的一种主要特性,即指植物经过弱毒性或另一个病原物的接种或一些化学物质诱导,经过7d左右后被接种的植物产生新的、广谱的系统抗性,从而对病原物再次侵染以及其它病菌的侵染均具有很强的抗性,该抗性水平可扩展到整个植株,故称为系统获得抗  相似文献   

8.
张茵 《中国农学通报》2007,23(6):504-504
近年来随着对植物抗病机理及信号转导途径的深入研究和探索,以及通过分子生物学手段新的抗病基因和病原菌无毒基因不断被克隆,科研人员对于植物三型信号分泌系统中抗病(R)基因和无毒(Avr)基因的结构、功能,作用模式及作用机制具有更加深入的认识。深入研究病原菌—寄主之间的相互作用关系,为制定更为有效的植物病害防治措施提供了依据。该文通过对三型信号分泌系统中植物病原识别受体的组成部分,抗病基因的结构域及种类,抗病基因与无毒基因及相互作用的两种模式及具体机制的总结,从植物抗病基因角度探讨了三型信号分泌系统下植物的抗病机制并在此基础上进行了前景展望。  相似文献   

9.
植物抗病分子机制研究进展   总被引:2,自引:0,他引:2  
李金玉  李冠  赵惠新  王贤雷  杜钰 《种子》2006,25(2):45-50
近十年来,植物抗病基因及其病原无毒基因的克隆,为在分子水平上揭示抗病基因的作用机制奠定了基础。本文综述了抗病基因作用的主要遗传基础模式,病原无毒基因及其蛋白产物的结构功能研究、植物抗病基因介导的信号传导以及抗病基因的潜能开发与应用,并对研究植物抗病机制的前景作了展望。  相似文献   

10.
《作物育种信息》2005,(8):11-11
水稻白叶枯病是由黄单孢杆菌Xarahomonas oryzoe pv.oryzae(简称Xoo)引起的,它是水稻最严重的病害之一。目前生产上还没有有效防治该病的措施,因而,培育抗病品种已成为农业科技工作者面临的一大课题。目前国内外对白叶枯病抗性机制的研究集中在三个方面:首先为病原菌的分子生物学研究,寻找病原菌的致病基因和无毒基因;其次为寄主植物的分子生物学研究,主要是对抗病基因进行定位、分离与克隆;再者为寄主植物与病原物之间相互作用的研究,研究植物防卫反应的信号传导途径。迄今,  相似文献   

11.
Richard N. Strange 《Euphytica》2006,147(1-2):49-65
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.  相似文献   

12.
植物抗病毒侵染的分子机制   总被引:2,自引:0,他引:2  
侯静  刘青青  徐明良 《作物学报》2012,38(5):761-772
植物病毒病是一类严重危害农作物生产的重要病害。已报道的植物抗病毒基因主要在抑制病毒增殖和阻止病毒扩散中起作用。病毒的复制涉及自身的编码蛋白及其与寄主蛋白间的互作, 参与病毒复制的寄主蛋白很多, 如真核翻译起始因子eIF4E和eIF4G, 植物的内膜系统等, 相关蛋白的功能丧失或构型改变可阻滞病毒的复制;此外, 植物细胞内的硫氧还蛋白可调节细胞的氧化还原状态, 进而阻断病毒的增殖。病毒在植物体内的扩散包括胞间移动和长距离迁移, 植物抗病蛋白(R蛋白)通过识别病毒的无毒因子(Avr)促发防御反应, 诱导过敏性坏死, 限制病毒在细胞间的扩散, 编码这类抗病蛋白的基因主要为TIR-NBS-LRR和CC-NBS-LRR。病毒的长距离迁移涉及的因素很多, 目前仅发现韧皮部的RTM蛋白可能以多聚蛋白的形式抵制病毒的长距离移动。另外, RNA沉默也是植物抵制病毒侵染的免疫反应机制。本文旨在综述植物的各种抗病毒机制和相关的抗病基因, 并探讨分子标记辅助选择(marker-assisted selection, MAS), 定向诱导基因组局部突变(targeting induced local lesions in genomes, TILLING)和转基因等生物技术在抗病改良中的应用前景。  相似文献   

13.
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.  相似文献   

14.
The fungus Cladosprium fulvum is a biotrophic leaf pathogen of tomato. The fungus develops in the intercellular space without forming specialized feeding structures and does not affect the leaf tissue. The outcome of the C. fulvum-tomato interaction can be described by the gene-for-gene model. Failure of infection is expressed by a hypersensitive response. Two fungal proteins, ECP1 and ECP2, have been isolated and their corresponding genes have been cloned. In a compatible interaction including many physiological races ECP1 and ECP2 are highly produced and a role in pathogenicity is suggestive. The ecp1 gene shows some homology with tumor necrosis factor receptors (TNFRs) while the ecp2 gene shows no homology with sequences known in data bases. However, disruption of one of the two genes showed no reduced pathogenicity of the fungus. Two race-specific elicitors, AVR4 and AVR9, have been isolated and their corresponding genes have been cloned. The avirulence genes Avr4 and Avr9 are only present in C. fulvum avirulent on Cf-4 and Cf-9 cultivars, respectively. The expression of these two genes is, like the expression of the ecp genes, highly induced when the fungus grows in planta. Disruption of the Avr9 gene in wild type avirulent races leads to virulence on tomato genotypes carrying the complementary resistance gene Cf-9. A single base-pair change in the avirulence gene Avr4 leads to virulence on tomato genotypes carrying the Cf-4 resistance gene. Isolation, characterization and possible function of ECP1, ECP2, AVR4, and AVR9 will be discussed.  相似文献   

15.
Specificity of interaction at the cotyledon stage was recently demonstrated between the blackleg pathogen, Leptosphaeria maculans, and Brassica napus. Three pathogenicity groups were distinguished, PG2 avirulent towards ‘Quinta’ and ‘Glacier’, PG3 avirulent towards ‘Quinta’, and PG4 virulent on the two cultivars. The genetic control of the interactions was investigated on both the pathogen and the plant. Tetrad analysis was performed following PG3 × PG4 and PG2 × PG4 crosses.‘Quinta’ and ‘Glacier’ were crossed with the susceptible winter oilseed rape cultivar ‘Score’. The analysis of F1, F2 and testcross populations suggested that the incompatible interaction between ‘Quinta’ and PG3 isolates is conditioned by the presence of the dominant single resistance allele Rlml in ‘Quinta’ and the matching avirulence gene AvrLml in L. maculans. Race-specific resistance of ‘Glacier’ to PG2 isolates was conditioned by the matching gene pair Rlm2/AvrLm2. Finally, the data suggest that two avirulence genes matching two dominant loci control the ‘Quinta’-PG2 interaction. The consequences of the occurrence of race-specific resistance in B. napus are discussed with respect to future breeding for blackleg resistance.  相似文献   

16.
植物广谱抗性反应中,特定的抗性基因通过细胞信号转导高度表达。应用图位克隆、转座子标签、微卫星标记等技术从一些主要的经济作物和园艺植物中定位和克隆了大量抗性基因。R蛋白是一类重要的Pr类蛋白,往往具有若干相似结构域,R蛋白结构和序列分析对抗性基因家族分类、抗性信号转导机制研究有重要意义。Avr基因研究的成果进一步证实了“基因对基因”学说。根据抗性细胞信号转导机制的研究,发展形成了激发子一受体学说、细胞防卫学说等一些新的植物抗性机制假说。目前已有十几种动植物、微生物的外源抗性基因应用于转基因植物研究中。  相似文献   

17.
Durability of resistance against potato cyst nematodes   总被引:1,自引:0,他引:1  
Jaap Bakker 《Euphytica》2002,124(2):157-162
A requirement for evaluating the effectiveness of major resistance genes (R-genes) is detailed knowledge of the genetic variability of the nematode populations in an area. Obtaining insight in the genetic variation in an area is a tour de force, because qualitative data are not sufficient allele frequency data at well studied loci are required. Another important step in predicting the durability of major R-genes is to study the parasite at the molecular level. Also for nematodes it seems that R-genes are part of a molecular surveillance system recognising foreign molecules. For potato cyst nematodes it is becoming clear that numerous proteins are secreted to manipulate the host plant and it may be assumed that some of these secretory proteins are also recognised by the host. Knowledge of the molecular nature and function of these avirulence gene products may reveal clues to predict the durability of an R-gene. R-genes that recognise avirulence gene products that have a crucial function in the nematode maybe very durable. When the current molecular models for gene-for-gene interactions are correct, the durability of an R-gene may be predicted by studying the dispensability factor and functional constraints of the avirulence gene products. This revised version was published online in August 2006 with corrections to the Cover Date.  相似文献   

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