Characterization of Signal Transduction Pathways in Plant Defense Responses

植物防御反应中信号转导途径的表征

• 批准号: 0110404
• 负责人: Daniel Klessig
• 金额: $ 60万
• 依托单位: Boyce Thompson Institute Plant Research
• 依托单位国家: 美国
• 项目类别: Continuing Grant
• 财政年份: 2001
• 资助国家: 美国
• 起止时间: 2001-09-01 至 2006-08-31
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=0110404&HistoricalAwards=false
• 关键词: Characterization; Signal; Transduction; Pathways; Plant

Numerous studies have demonstrated that salicylic acid (SA), jasmonic acid (JA) and ethylene play key roles in activation of various defense responses following pathogen attack. Induction of SA-mediated responses occurs via both NPR1- dependent and -independent pathways. The SA- and JA/ethylene-mediated pathways appear to be coordinately regulated with extensive cross-talk occurring between them. The nature of this cross-talk is poorly understood and may involve complex regulatory mechanisms. In addition, environmental factors can significantly and sometimes dramatically influence the outcome of plant-pathogen interactions; the molecular and cellular basis for these effects is largely unknown.Two groups of Arabidopsis mutants have been isolated whose initial characterization argues that they will provide important insights into the molecular mechanisms underlying (i) the NPR1- dependent vs -independent pathway(s), (ii) the cross-talk between the SA- and JA/ethylene- mediated pathways and (iii) the effects of environment on disease resistance. The discovery that the fatty acid 18:1, or a derivative of it, functions as a signal together with JA to activate expression of the defensin gene PDF1.2, but suppresses SA-dependent defense response is particularly exciting. This co-activating signal was uncovered in the ssi2 mutant. ssi2 suppresses salicylate insensitivity of the npr1-5 mutant due to a mutation in a stearoyl-ACP desaturase which results in reduced fatty acid desaturation. One of the highest priorities is to determine whether 18:1 itself, or rather a derivative of it, is the co-activating signal. Suppressor mutants of ssi2 will also be isolated in order to better characterize the co-activating signal and its role in modulating defense responses.The genes for two other ssi mutants, ssi1 and ssi4, have been cloned. In addition to isolating suppressors of each, it will be determined whether the function of other genes shown to have a role in SA signaling (ed. PAD3 or PAD4), JA/ ethylene signaling (eg. COI1 or ETR1) or R gene-mediated signaling (eg. NDR1 or EDS1) are required for some or all of the mutant phenotypes.The second group of mutants constitutively expresses pathogenesis-related genes (cpr). cpr22, also exhibit SA-dependent (i) lesion formation, (ii) enhanced disease resistance and (iii) homozygous lethality as well as JA/ ethylene-mediated constitutive PDF1.2 gene expression. Interestingly, the SA -dependent, but not JA-mediated, phenotypes are suppressed by high relative humidity (RH). High RH also suppresses the SA-dependent phenotype of ssi4. In addition, ssi4 is extremely cold sensitive, with death occurring at 16 degrees C. Thus, further characterization of cpr22 and ssi4 by conducting epistatic analyses and/or isolating suppressor mutants for each of these pathways should provide valuable insights into how environmental factors (RH and temperature) influence disease resistance. It should be noted that SA may also play a signaling role in other processes, including thermogenesis, cell growth and trichome development. Thus, elucidation of the components involved in the SA defense signaling pathways may well provide insights into a much larger signaling network through which plants regulate a wide variety of responses.

大量研究表明，水杨酸（SA）、茉莉酸（JA）和乙烯在病原菌攻击后激活各种防御反应中起着关键作用。SA介导的反应的诱导通过NPR 1依赖性和非依赖性途径发生。SA-和JA/乙烯介导的途径似乎是协调调节与它们之间发生广泛的串扰。这种串扰的性质知之甚少，可能涉及复杂的调节机制。此外，环境因素可以显著地、有时是戏剧性地影响植物-病原体相互作用的结果;这些作用的分子和细胞基础在很大程度上是未知的。已经分离了两组拟南芥突变体，其初步表征表明它们将为以下分子机制提供重要的见解：（i）NPR 1依赖性途径vs非依赖性途径，（ii）SA-和JA/乙烯-介导的途径之间的串扰和（iii）环境对抗病性的影响。特别令人兴奋的发现是，脂肪酸18：1或其衍生物与JA一起作为信号激活防御素基因PDF1.2的表达，但抑制SA依赖性防御反应。这种共激活信号在ssi 2突变体中被发现。ssi 2抑制npr 1 -5突变体的水杨酸不敏感性，这是由于硬脂酰-ACP去饱和酶的突变导致脂肪酸去饱和减少。最高优先级之一是确定18：1本身或其衍生物是否是共激活信号。为了更好地描述共激活信号及其在调节防御反应中的作用，我们还将分离出ssi 2的抑制突变体，另外两个ssi突变体，ssi 1和ssi 4的基因也已克隆。除了分离每种的抑制子之外，还将确定显示在SA信号传导（编辑PAD 3或PAD 4）、JA/乙烯信号传导（例如PAD 4）中具有作用的其他基因的功能是否与SA信号传导（编辑PAD 3或PAD 4）、JA/乙烯信号传导（编辑PAD 4）和JA/乙烯信号传导（编辑PAD 4）中具有作用的其他基因的功能。COI 1或ETR 1）或R基因介导的信号传导（例如，NDR 1或EDS 1）是部分或全部突变体表型所必需的。第二组突变体组成型表达病程相关基因（cpr）。cpr 22也表现出SA依赖性（i）损伤形成，（ii）增强的抗病性和（iii）纯合致死性以及JA/乙烯介导的组成型PDF1.2基因表达。有趣的是，SA依赖性，但不是JA介导的，表型被高相对湿度（RH）抑制。高RH也抑制SA依赖表型的ssi 4。此外，ssi 4对寒冷非常敏感，在16摄氏度时死亡。因此，cpr 22和ssi 4的进一步表征进行上位性分析和/或分离这些途径的抑制突变体应该提供有价值的见解如何环境因素（RH和温度）影响抗病性。 应当指出的是，SA还可以在其他过程中发挥信号作用，包括产热、细胞生长和毛状体发育。因此，阐明参与SA防御信号通路的组件可以很好地提供洞察到一个更大的信号网络，通过该网络植物调节各种各样的反应。