活性氧中间体和NO在植物抗病中的作用

植物与病原菌互作时,活性氧中间体(reactiveoxygenintermediates,ROI)和一氧化氮(NO)参与了植物抗病性的建立。寄主与病原菌非亲合性互作产生二次氧爆发高峰,体内NO增加。许多氧化酶可以催化氧爆发产生ROI。ROI和NO通过氧化还原信号启动寄主细胞局部的过敏性坏死反应和全株系统获得性抗病性。     

植物氮素营养与病害发生关系研究进展

氮素营养不仅影响植物的正常生长发育,还会影响植物的感病性或抗病性。该文主要综述了氮素营养及其代谢对植物病害发展的影响、诱导病原菌侵染的寄主氮营养信号和氮素营养对植物与病原菌互作相关基因表达的影响,尤其是氮素受限(饥饿)对病原菌基因的诱导表达、植物衰老基因和抗病基因的关系、植物衰老过程中防御基因的表达等国际研究的热点领域所取得的成果和进展,并讨论了有待深入研究的问题。     

植物抗病的信号转导途径

植物在遭受不同病原菌入侵时会表现出不同的反应,若病原菌具有逃避寄主的识别并破坏寄主防御系统的能力则表现感病;若植物能及时识别病原菌并激活自身的防御体系,将表现出抗病性,而特异性的抗病性常常伴有过敏反应的产生。那么植物对病原菌的最初识别,识别后的信号转导以及抗病性过程究竟是怎样的呢？本文将对这一问题进行概述。     

植物抗病反应的信号传导网络

植物由抗病基因介导的防卫过程存在一系列生理生化和分子生物学反应,这些反应从病原菌侵染点开始的超敏反应(HR)并延伸到远处组织的系统抗性或获得性抗性(SAR),受制于一种信号传导网络的调控。这个信号系统由抗病蛋白和病原菌非毒性蛋白在一种配体-受体的互作模式下激发,并由信号分子H2O2,NO和系统信号分子SA,JA和乙烯和通过关键调控基因传递和放大,最终诱导一系列防卫反应基因的表达和代谢的变化而产生抗性。植物防卫信号的产生有类似于动物免疫系统因子的介导,并可由非寄主病原菌或诱导子诱发。这些信号途径所产生的广谱抗性为植物抗病基因工程的应用奠定了基础。     

植物抗病反应的信号传导网络

植物由抗病基因介导的防卫过程存在一系列生理生化和分子生物学反应,这些反应从病原菌侵染点开始的超敏反应（HR）并延伸到远处组织的系统抗性或获得性抗性（SAR）,受制于一种信号传导网络的调控,这个信号系统由抗病蛋白和病原菌非毒性蛋白在一种配体-受体的互作模式下激发,并由信号分子H2O2,NO和系统信号分子SA,JA和乙烯和通过关键调控基因传递和放大,最终诱导一系列防卫反应基因的表达和代谢的变化而产生抗性。植物防卫信号的产生有类似于动物免疫系统因子的介导,并可由非寄主病原菌或诱导子诱发,这些信号途径所产生的广谱抗性为植物抗病基因工程的应用奠定了基础。     

抗氰交替途径对寄主植物感病性的调节

马铃薯块茎切片－ 软腐病菌亲和互作过程中, 不同强度的亲和互作中活性氧的释放有其不同的特点。在强亲和互作中的２４ 小时内,无明显的活性氧释放。但在弱亲和互作中,互作８ 小时后,即有明显的活性氧的释放,２０ 小时达到高峰,并且这种活性氧的释放提高寄主的抗病性。试验显示马铃薯块茎切片与软腐病菌的亲和互作诱导寄主抗氰交替途径的运行,ＳＨＡＭ 处理降低亲和互作过程中寄主的感病性, 同时ＳＨＡＭ 处理也促进亲和互作中寄主活性氧释放高峰的出现, 表明抗氰交替途径的运行可通过抑制亲和互作中寄主活性氧的产生而促进寄主的感病性。从而证明了一种新的寄主植物抗感病反应机制     

植物与病原菌互作的蛋白质组学研究进展

深入认识植物与病原菌的识别方式、亲和性或非亲和性的互作模式,对于揭示植物-病原菌互作机制研究具有重要意义.利用蛋白质组学方法研究病原菌侵染植物过程,分析相关的基因和蛋白,有助于从分子水平上探究植物-病原菌相互作用机制.本文概述了植物-病原菌的互作机制,系统介绍了差异蛋白质组学分析方法在植物-病原真菌、植物-病原细菌两类互作系统中的应用,分析了植物与病原菌互作过程中可能涉及的差异表达功能蛋白,并对当前蛋白质组学技术在植物与病原菌互作研究中存在的诸多问题进行了探讨.     

大豆疫霉与大豆互作中的识别与反识别

大豆疫霉引起的大豆疫病是大豆生产上的毁灭性病害。深入了解大豆疫霉与寄主在分子层面的互作机制是解析病原菌致病机理、针对性地制定防治措施的必要前提。目前研究表明,植物通过两个层面的识别机制来启动防卫反应,而能否正确识别"非我"分子则是植物开启免疫系统的关键。而对于病原菌,则采用多种分子策略来极力逃避寄主的识别机制,分泌效应分子协同抑制寄主免疫反应。本文综述了一系列大豆抗病基因介导的小种专化抗性丧失的原因,以及大豆疫霉效应分子逃避和破坏寄主免疫反应的分子策略,并讨论了基于这些分子互作机制应用于筛选新型抗病资源和精确育种的可能性。     

ROS信号对植物抗性的调控作用研究进展

活性氧(reactive oxygen species,ROS)是植物体代谢所产生的小分子化合物,既是生长发育和防御途径的关键调节因子,又是需氧代谢的有毒副产物。植物细胞的生理过程受一个被活性氧调节的氧化还原网状途径的调控,本文从植物体内ROS产生的部位与时空特异性、ROS信号与NO和Ca2+波信号的互作等方面综述了ROS信号对植物抗性的调控作用研究进展。     

马铃薯Y病毒属病毒与寄主互作的分子基础*

近年来 ,分子生物学及生物技术的迅速发展 ,极大地促进了人们对马铃薯Y病毒属病毒与寄主之间 ,病毒与传播介体之间互作关系的研究 ,并取得了一些新的进展。从病毒诱导的症状 ,病毒的系统侵染、传播以及寄主植物抗病性等方面 ,对病毒与寄主互作关系的分子基础作一简述。     

壳寡糖、一氧化氮和植物激素在烟草气孔运动中的作用及其相互关系

本文研究了壳寡糖（COS）、一氧化氮（NO）和植物激素对烟草气孔运动的作用及其相互关系,结果表明,COS、NO、脱落酸（ABA）能诱导烟草气孔开度减小;ABA合成抑制剂钨酸钠（Na2WO4）和NO合成酶抑制剂L-NAME具有清除COS、ABA或NO诱导烟草气孔开度减小的作用。说明COS通过诱导ABA和NO产生,进而诱导烟草气孔开度减小,而且ABA和NO之间有相互作用。另外,细胞分裂素和生长素能够诱导烟草气孔开度增大,也能够逆转COS诱导的气孔开度减小。     

La（NO3）3浸种对NaCl胁迫下红小豆幼苗生长的影响

采用向1／2Hoagland营养液中按一定比例添加中性盐（NaCl）模拟盐胁迫的方式,研究了h（NO3）,浸种对盐胁迫下红小豆（Phaseolus angularis）幼苗生长的影响。结果表明：（1）与对照组相比,盐胁迫不同程度地降低了红小豆幼苗的株高、叶面积、地上部分鲜重、总根数及根系活力、根苗SOD、POD、CAT活性等,明显增加了根苗MDA含量水平。（2）使用适当浓度的La（NO3）3浸种可以提高对照组和盐处理组红小豆的株高、叶面积、总根长、总根数、叶绿素、根活力及SOD、POD和CAT活性,也可以显著降低根苗MDA含量水平,且大多表现出在盐胁迫下变化幅度高于正常处理。La（NO3）3浸种有利于缓解盐胁迫带来的不良影响。（3）低浓度的La（NO3）3浸种处理能够提高红小豆幼苗的耐盐性,缓解盐胁迫伤害,而高浓度处理则加剧了盐胁迫伤害。30mg／L La（NO3）3浸种对提高红小豆幼苗耐盐性的效果最好。     

Genetic elucidation of nitric oxide signaling in incompatible plant-pathogen interactions

Recent experiments indicate that nitric oxide (NO) plays a pivotal role in disease resistance and several other physiological processes in plants. However, most of the current information about the function of NO in plants is based on pharmacological studies, and additional approaches are therefore required to ascertain the role of NO as an important signaling molecule in plants. We have expressed a bacterial nitric oxide dioxygenase (NOD) in Arabidopsis plants and/or avirulent Pseudomonas syringae pv tomato to study incompatible plant-pathogen interactions impaired in NO signaling. NOD expression in transgenic Arabidopsis resulted in decreased NO levels in planta and attenuated a pathogen-induced NO burst. Moreover, NOD expression in plant cells had very similar effects on plant defenses compared to NOD expression in avirulent Pseudomonas. The defense responses most affected by NO reduction during the incompatible interaction were decreased H(2)O(2) levels during the oxidative burst and a blockage of Phe ammonia lyase expression, the key enzyme in the general phenylpropanoid pathway. Expression of the NOD furthermore blocked UV light-induced Phe ammonia lyase and chalcone synthase gene expression, indicating a general signaling function of NO in the activation of the phenylpropanoid pathway. NO possibly functions in incompatible plant-pathogen interactions by inhibiting the plant antioxidative machinery, and thereby ensuring locally prolonged H(2)O(2) levels. Additionally, albeit to a lesser extent, we observed decreases in salicylic acid production, a diminished development of hypersensitive cell death, and a delay in pathogenesis-related protein 1 expression during these NO-deficient plant-pathogen interactions. Therefore, this genetic approach confirms that NO is an important regulatory component in the signaling network of plant defense responses.     

外源NO对铜胁迫下番茄幼苗根系构型及其超微结构的影响

采用营养液水培的方法,以“改良毛粉802F1”番茄为材料,硝普钠（sodiumnitroprusside,sNP）为一氧化氮（N0）供体,研究外源N0对铜胁迫下番茄幼苗根系构型及其超微结构的影响。结果表明,50μmol·L-1的铜胁迫下,外施100μmol·L-1 SNP能够显著增加番茄幼苗植株的生物量、株高和茎粗,提高根系活力,改善根系构型中的根长度、根平均直径、根表面积和根体积,缓解番茄幼苗亚细胞结构（细胞核、线粒体、叶绿体、液泡、核膜）的改变,维持番茄幼苗组织结构的稳定,减缓铜胁迫对植株生长的抑制作用,添加NO清除剂牛血红蛋白后,能显著消除NO的缓解效果。     

NO way to live; the various roles of nitric oxide in plant-pathogen interactions

Nitric oxide has attracted considerable interest from plant pathologists due its established role in regulating mammalian anti-microbial defences, particularly via programmed cell death (PCD). Although NO plays a major role in plant PCD elicited in response to certain types of pathogenic challenge, the race-specific hypersensitive response (HR), it is now evident that NO also acts in the regulation of non-specific, papilla-based resistance to penetration by plant cells that survive attack and, possibly, in systemic acquired resistance. Equally, the potential roles of NO signalling/scavenging within the pathogen are being recognized. This review will consider key defensive roles played by NO in living cells during plant-pathogen interactions, as well as in those undergoing PCD.     

Nitric oxide function and signalling in plant disease resistance

Nitric oxide (NO) is one of only a handful of gaseous signalling molecules. Its discovery as the endothelium-derived relaxing factor (EDRF) by Ignarro revolutionized how NO and cognate reactive nitrogen intermediates, which were previously considered to be toxic molecules, are viewed. NO is now emerging as a key signalling molecule in plants, where it orchestrates a plethora of cellular activities associated with growth, development, and environmental interactions. Prominent among these is its function in plant hypersensitive cell death and disease resistance. While a number of sources for NO biosynthesis have been proposed, robust and biologically relevant routes for NO production largely remain to be defined. To elaborate cell death during an incompatible plant-pathogen interaction NO functions in combination with reactive oxygen intermediates. Furthermore, NO has been shown to regulate the activity of metacaspases, evolutionary conserved proteases that may be intimately associated with pathogen-triggered cell death. NO is also thought to function in multiple modes of plant disease resistance by regulating, through S-nitrosylation, multiple nodes of the salicylic acid (SA) signalling pathway. These findings underscore the key role of NO in plant-pathogen interactions.     

脂多糖诱导植物细胞产生NO的光学分子成像检测

脂多糖（lipopolysaccharides, LPS）是革兰氏阴性细菌细胞壁的主要成分,被植物感知后,启动植物防御反应。利用荧光探针分子成像及激光共聚焦扫描显微镜技术,在位、直观检测了LPS诱导下,拟南芥细胞产生重要信号分子一氧化氮（ NO）的时空特征。LPS诱导细胞产生大量NO,这些NO主要定位在细胞膜周围,且是在LPS处理90 min后出现。NO合成酶抑制剂L-单甲基精氨酸能明显抑制LPS诱导的NO生成,说明LPS诱导NO产生是NO合成酶途径依赖的。该研究结果有助于深入理解LPS作用机制以及NO信号传导通路的全貌,并为生物物理技术在相关植物生理研究中的应用提供一定的借鉴作用。     

植物细胞一氧化氮信号转导研究进展

一氧化氮（nitric oxide,NO）作为重要的信号分子,调控植物的种子萌发、根形态建成和花器官发生等许多生长发育过程,并参与气孔运动的调节以及植物对多种非生物胁迫和病原体侵染的应答过程。已经知道,精氨酸依赖的NOS途径和亚硝酸盐依赖的NR途径是植物细胞NO产生的主要酶促合成途径。NO及其衍生物能够直接修饰底物蛋白的金属基团、半胱氨酸和酪氨酸残基,通过金属亚硝基化、巯基亚硝基化和Tyr．硝基化等化学修饰方式,调节靶蛋白的活性,并影响cGMP和Ca2＋信使系统等下游信号途径,调控相应的生理过程。最新的一些研究结果也显示,MAPK级联系统与NO信号转导途径之间存在复杂的交叉调控。此外,作为活跃的小分子信号,NO和活性氧相互依赖并相互影响,共同介导了植物的胁迫应答和激素响应过程。文章综述了植物NO信号转导研究领域中一些新的研究进展,对NO与活性氧信号途径间的交叉作用等也作了简要介绍。     

Local and systemic production of nitric oxide in tomato responses to powdery mildew infection

Various genetic and physiological aspects of resistance of Lycopersicon spp. to Oidium neolycopersici have been reported, but limited information is available on the molecular background of the plant–pathogen interaction. This article reports the changes in nitric oxide (NO) production in three Lycopersicon spp. genotypes which show different levels of resistance to tomato powdery mildew. NO production was determined in plant leaf extracts of L. esculentum cv. Amateur (susceptible), L. chmielewskii (moderately resistant) and L. hirsutum f. glabratum (highly resistant) by the oxyhaemoglobin method during 216 h post-inoculation. A specific, two-phase increase in NO production was observed in the extracts of infected leaves of moderately and highly resistant genotypes. Moreover, transmission of a systemic response throughout the plant was observed as an increase in NO production within tissues of uninoculated leaves. The results suggest that arginine-dependent enzyme activity was probably the main source of NO in tomato tissues, which was inhibited by competitive reversible and irreversible inhibitors of animal NO synthase, but not by a plant nitrate reductase inhibitor. In resistant tomato genotypes, increased NO production was localized in infected tissues by confocal laser scanning microscopy using the fluorescent probe 4-amino-5-methylamino-2',7'-difluorofluorescein diacetate. NO production observed in the extracts from pathogen conidia, together with elevated NO production localized in developing pathogen hyphae, demonstrates a complex role of NO in plant–pathogen interactions. Our results are discussed with regard to a possible role of increased NO production in pathogens during pathogenesis, as well as local and systemic plant defence mechanisms.