水杨酸诱导普通菜豆镰孢菌枯萎病抗病性的研究

普通菜豆是人类主要食用豆类之一,其营养价值高、栽培面积大。镰孢菌枯萎病是普通菜豆典型的土传病害,给普通菜豆生产带来严重损失。水杨酸(SA)被认为是诱导植物抗病反应的重要信号分子之一,参与植物的过敏反应(HR)和系统获得性抗性反应(SAR)。本研究通过不同植物激素处理普通菜豆BRB-130,结果表明,SA处理普通菜豆叶片使植株根中SA的含量升高,并显著提高植株对枯萎病原菌FOP-DM01菌株的抗性。SA诱导普通菜豆根组织中苯丙氨酸解氨酶、过氧化物酶活性及过氧化氢的含量显著升高,从而诱导普通菜豆产生HR和SAR。因此,SA作为普通菜豆抗病信号途径中重要的化学激活因子,能够显著提高普通菜豆对枯萎病原菌的抗病性,为发展环境友好型化学农药提供新的思路。     

脂氧合酶、茉莉酸和水杨酸对猕猴桃果实后熟软化进程中乙烯生物合成的调控

20℃下后熟果实的LOX活性增加先于自由基产生和乙烯生成;JA处理对果实后熟软化启动期(采后1d)和果实快速软化期(采后5d)果实切片中的LOX活性、自由基产生和乙烯生物合成有促进作用,至果实软化后期(采后7d)这种效应消失;亚油酸只在采后1d果实切片中促使LOX活性和乙烯生成;SA处理抑制了果实后熟进程中组织切片的LOX活性、自由基产生和乙烯的生物合成;SA和JA对LOX活性和乙烯生物合成具有明显的拮抗作用。     

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。     

钙对水杨酸诱导番茄叶片灰霉病抗性及防御酶活性的影响

以番茄‘L402’品种幼苗为试材,经水杨酸(SA)诱导处理后接种灰霉病菌,再进行外源Ca2+、Ca2+螯合剂和Ca2+抑制剂处理,分析Ca2+和SA处理番茄叶片对灰霉病抗性和主要防御酶系活性的变化,探讨Ca2+和SA对番茄诱导抗病性的影响。结果显示:(1)外源SA可显著提高番茄诱导叶和非诱导叶抗灰霉病能力,Ca2+能进一步增强SA诱导的抗病能力;而Ca2+螯合剂EGTA和质膜钙通道抑制剂LaCl3则不同程度地抑制了SA诱导的番茄灰霉病抗性。(2)外源SA能提高番茄诱导叶和非诱导叶中苯丙氨酸解氨酶(PAL)、多酚氧化酶(PPO)、过氧化物酶(POD)活性,外源Ca2+亦进一步增强了SA诱导的上述防御酶活性,但缺钙处理则不同程度降低这些防御酶活性。(3)外源补充Ca2+及不同缺钙处理对SA诱导的过氧化氢酶(CAT)和超氧化物歧化酶(SOD)活性未发现规律性影响。研究表明,钙对SA诱导番茄抗灰霉病性的增强效应,可能与其提高SA诱导番茄叶片中PAL、PPO和POD等防御酶活性有关。     

采前壳寡糖处理对杏果实黑斑病的抗性诱导

以新疆赛买提杏为试验材料,分别在果实坐果期、膨大期、转色期及采收前48h,采用分子量为5 000、浓度为0.05%的壳寡糖(GOS)溶液对杏果实进行喷施处理,以喷施清水为对照(CK);采收后的杏果实在机械损伤接种链格孢菌后置于4℃、相对湿度90%~95%的条件下贮藏,定期统计接种链格孢菌杏果实的病斑直径和发病率,测定抗病相关酶苯丙氨酸解氨酶(PAL)、β-1,3-葡聚糖酶(GLU)和几丁质酶(CHT)的活性及木质素、富含羟脯氨酸糖蛋白(HRGP)的含量,探讨采前壳寡糖处理对杏果实黑斑病的抗性诱导及其生理机制。结果显示,贮藏结束时,采前壳寡糖处理的果实发病率与病斑直径分别比对照显著降低了16.37%和17.57%。随着贮藏期间的延长,壳寡糖处理杏果实PAL、GLU、CHT的活性和木质素、HRGP的含量均表现出先上升后下降的变化趋势,且始终显著高于同期对照,并分别在接种后第21、28、21、28和14天达到峰值,峰值比同期对照分别显著提高12.17%、78.22%、31.41%、34.81%和77.44%。研究表明,采前壳寡糖处理能通过诱导提高杏果实病程相关蛋白及细胞壁HRGP和木质素的含量来增强杏果实对黑斑病的抗性。     

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。     

水杨酸诱导小白菜抗霜霉病的作用研究

以小白菜(Brassica campestris ssp.chinesis L.)为材料,采用叶面喷洒的方法施用不同浓度水杨酸(Salicylic acid,SA),研究了SA小白菜对霜霉病的抗性诱导,并对经SA诱导后小白菜植株体内相关酶活性进行了研究.结果发现,在0.2～2.0 mmol·L-1的浓度范围内,随着SA浓度的增加,SA的诱导防治效果先增后减,1.0 mmol·L-1浓度为诱导抗性最适浓度.经SA诱导后,小白菜植株体内SOD、POD和PPO等酶活性也明显增强.     

丁香精油对冷藏冬枣果实腐烂及诱导抗病相关酶活性的影响

对不同浓度丁香精油处理冬枣果实在0℃贮藏期间(60d)及藏后25℃货架期(5d)的果实腐烂率、诱导抗病相关酶活性和总酚含量的变化特征进行分析,以探索丁香精油抑制冬枣果实腐烂与抗病性诱导的关系。结果表明:丁香精油处理能有效抑制冬枣贮藏期果实腐烂的发生,提高其苯丙氨酸解氨酶、多酚氧化酶和过氧化物酶活性,诱导总酚含量的增加。经丁香精油处理冬枣果实在贮藏60d后25℃货架期5d时的腐烂指数得到明显下降,同时保持了较高的苯丙氨酸解氨酶、多酚氧化酶、过氧化物酶活性和总酚含量,并以0.50%丁香精油处理的效果最显著,其贮藏后货架期的果实腐烂指数较对照下降了45.5%。可见,丁香精油抑制贮藏冬枣果实的腐烂与抗病相关酶活性的升高密切相关,抗病性诱导是丁香精油处理抑制冬枣采后果实腐烂的重要原因之一。     

纯氧对采后杨梅果实腐烂的抑制与抗病相关酶的诱导

为研究高氧对抑制果实腐烂的作用及其与抗病相关酶活性诱导的关系,将杨梅果实采后在5℃用纯氧或空气(对照)处理12 d.结果表明,纯氧处理可显著抑制果实腐烂发生,贮藏12 d后对照果实的腐烂指数达到54%,而处理果实仅为17%.纯氧处理在贮藏前期可诱导杨梅果实几丁质酶和β-1,3-葡聚糖酶活性的升高,并在第6天时达到高峰.另外,纯氧处理增加了苯丙氨酸解氨酶和过氧化物酶的活性及总酚含量,并在整个贮藏期间一直高于对照水平.这些结果表明,高氧抑制杨梅果实腐烂的作用与诱导与抗病相关的酶的活性升高密切相关,抗病性诱导是高氧抑制杨梅果实腐烂的重要原因.     

植物系统获得性抗性的信号转导

坏死病原菌（necrotizingpathogen）的侵染或者一些化学因子的处理能诱导植物的非侵染或非处理部位产生对多种病原再侵染产生抗性,即系统获得性抗性（systemicacquiredresistance,SAR）。获得系统抗性的组织中SAR基因产物的累积和防卫反应的潜在诱导增强（potentiation）是其两类抗病机制。SAR至少有通过水杨酸（salicylicacid,SA）或茉莉酸（jasmonicacid,JA）、乙烯（ethylene）为系统信号分子的两类信号转导途径。遗传分析已用于SAR产生的信号转导过程的分析,一些与SAR信号转导相关的基因已经和正在克隆,这些基因具有明显提高植物广谱抗性的潜能。     

Interacting signal pathways control defense gene expression in Arabidopsis in response to cell wall-degrading enzymes from Erwinia carotovora

We have characterized the role of salicylic acid (SA)-independent defense signaling in Arabidopsis thaliana in response to the plant pathogen Erwinia carotovora subsp. carotovora. Use of pathway-specific target genes as well as signal mutants allowed us to elucidate the role and interactions of ethylene, jasmonic acid (JA), and SA signal pathways in this response. Gene expression studies suggest a central role for both ethylene and JA pathways in the regulation of defense gene expression triggered by the pathogen or by plant cell wall-degrading enzymes (CF) secreted by the pathogen. Our results suggest that ethylene and JA act in concert in this regulation. In addition, CF triggers another, strictly JA-mediated response inhibited by ethylene and SA. SA does not appear to have a major role in activating defense gene expression in response to CF. However, SA may have a dual role in controlling CF-induced gene expression, by enhancing the expression of genes synergistically induced by ethylene and JA and repressing genes induced by JA alone.     

PAD4 functions upstream from salicylic acid to control defense responses in Arabidopsis.

The Arabidopsis PAD4 gene was previously shown to be required for synthesis of camalexin in response to infection by the virulent bacterial pathogen Pseudomonas syringae pv maculicola ES4326 but not in response to challenge by the non-host fungal pathogen Cochliobolus carbonum. In this study, we show that pad4 mutants exhibit defects in defense responses, including camalexin synthesis and pathogenesis-related PR-1 gene expression, when infected by P. s. maculicola ES4 326. No such defects were observed in response to infection by an isogenic avirulent strain carrying the avirulence gene avrRpt2. In P. s. maculicola ES4 326-infected pad4 plants, synthesis of salicylic acid (SA) was found to be reduced and delayed when compared with SA synthesis in wild-type plants. Moreover, treatment of pad4 plants with SA partially reversed the camalexin deficiency and PR-1 gene expression phenotypes of P. s. maculicola ES4 326-infected pad4 plants. These findings support the hypothesis that PAD4 acts upstream from SA accumulation in regulating defense response expression in plants infected with P. s. maculicola ES4 326. A working model of the role of PAD4 in governing expression of defense responses is presented.     

Salicylic acid and the plant pathogen Erwinia carotovora induce defense genes via antagonistic pathways

Infection of tobacco plants with the plant pathogenic bacterium Erwinia carotovora subsp. carotovora or treatment of plants with Erwinia -derived elicitor preparations leads to the induction of a number of genes thought to play a role in plant defense response to pathogens. In order to determine the role of salicylic acid (SA) in the induction of the Erwinia responsive genes, the accumulation of mRNAs for these and other genes encoding pathogenesis-related proteins (PR genes) in response to both Erwinia elicitors and SA was determined. PR genes were identified which were preferentially induced by Erwinia elicitor preparations, one gene was induced by SA but not by Erwinia , and another gene was induced by both type of treatments. The differential expression of these genes and the timing of induction suggest that SA is not the signal molecule leading to the early response of plants to Erwinia . This was demonstrated by experiments using transgenic NahG plants that overproduce a salicylate hydroxylase inactivating SA. The elicitation of PR genes by Erwinia was similar in NahG and wild-type plants. Therefore, induction of plant defense genes by Erwinia and SA seems to be by two distinct pathways leading to expression of separate sets of genes. Furthermore, we could demonstrate that Erwinia elicitors antagonize the SA-mediated induction of PR genes. Similarly, SA appeared to inhibit the induction of PR genes elicited by Erwinia . The observed antagonism between the two signal transduction pathways indicates the presence of a common regulatory element in both pathways that acts downstream of SA in the SA-mediated response.     

Enhanced Disease Susceptibility 1 and Salicylic Acid Act Redundantly to Regulate Resistance Gene-Mediated Signaling

Resistance (R) protein–associated pathways are well known to participate in defense against a variety of microbial pathogens. Salicylic acid (SA) and its associated proteinaceous signaling components, including enhanced disease susceptibility 1 (EDS1), non–race-specific disease resistance 1 (NDR1), phytoalexin deficient 4 (PAD4), senescence associated gene 101 (SAG101), and EDS5, have been identified as components of resistance derived from many R proteins. Here, we show that EDS1 and SA fulfill redundant functions in defense signaling mediated by R proteins, which were thought to function independent of EDS1 and/or SA. Simultaneous mutations in EDS1 and the SA–synthesizing enzyme SID2 compromised hypersensitive response and/or resistance mediated by R proteins that contain coiled coil domains at their N-terminal ends. Furthermore, the expression of R genes and the associated defense signaling induced in response to a reduction in the level of oleic acid were also suppressed by compromising SA biosynthesis in the eds1 mutant background. The functional redundancy with SA was specific to EDS1. Results presented here redefine our understanding of the roles of EDS1 and SA in plant defense.     

Constitutive salicylic acid-dependent signaling in cpr1 and cpr6 mutants requires PAD4

Salicylic acid (SA)-dependent signaling controls activation of a set of plant defense mechanisms that are important for resistance to a variety of microbial pathogens. Many Arabidopsis mutants that display altered SA-dependent signaling have been isolated. We used double mutant analysis to determine the relative positions of the pad4, cpr1, cpr5, cpr6, dnd1 and dnd2 mutations in the signal transduction network leading to SA-dependent activation of defense gene expression and disease resistance. The pad4 mutation causes failure of SA accumulation in response to infection by certain pathogens, while the other mutations cause constitutively high levels of SA, defense gene expression and resistance. The cpr1 pad4, cpr5 pad4, cpr6 pad4, dnd1 pad4 and dnd2 pad4 double mutants were constructed and assayed for stature, presence of spontaneous lesions, resistance to Pseudomonas syringae and Peronospora parasitica, SA levels, expression of PAD4, PR-1 and PDF1.2, and accumulation of camalexin. We found that the effects of the cpr1 and cpr6 mutations on SA-dependent gene expression are completely dependent on PAD4 function. In contrast, SA accumulation in the lesion-mimic mutant cpr5 is partially PAD4-independent, while in dnd1 and dnd2 mutants it is completely PAD4-independent. A model describing a possible arrangement of activities in the signal transduction network is presented.