Characterization of Negative Regulators of NPR1-Mediated Systemic Acquired Resistance

NPR1 介导的系统获得性耐药性负调节因子的表征

• 批准号: 0090887
• 负责人: Xinnian Dong
• 金额: $ 52万
• 依托单位: Duke University
• 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: 2001-02-15 至 2006-01-31
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=0090887&HistoricalAwards=false
• 关键词: Characterization; Negative; Regulators; NPR1; Mediated

The long-term goal of this research is to use Arabidopsis thaliana as amodel system to determine the signaling events leading to systemic acquiredresistance (SAR). SAR is a secondary pathogen resistance which can beinduced after a local infection. SAR is broad-spectrum and long-lasting.Through genetic screens, NPR1 has been identified as a key positiveregulator of SAR; mutants of the NPR1 gene are nonresponsive to SARinduction. NPR1 encodes a novel protein with functionally importantprotein-protein interacting domains, the BTB domain and the ankyrin-repeatdomain. Recent data show that nuclear localization of NPR1 is essentialfor its function. In the nucleus, NPR1 may affect the activities of theTGA subclass of bZIP transcription factors as well as the WRKYtranscription factors, which have been implicated as transcriptionalactivators and repressors of pathogenesis-related (PR) genes, respectively.A genetic screen for suppressors of npr1 has led to identification of sni1,a mutation that restores systemic induction of PR genes in npr1. Thewild-type SNI1 is believed to be a negative regulator of SAR whoseinactivation requires the function of NPR1. It is hypothesized that NPR1induces SAR by activating the TGA transcription activators and inactivatingWRKY transcription repressors, and relieving the negative control of SNI1.In this project, molecular genetic and biochemical experiments are designedto (1) determine the functional significance of the interaction betweenNPR1 and WRKY transcription factors in SAR; (2) determine the mechanism bywhich SNI1 functions as a negative regulator of SAR; and (3) identifycomponents in the NPR1-complex. Because NPR1, SNI1, and WRKY transcriptionfactors are either novel or plant-specific proteins, characterization ofthese components may unveil new mechanisms of signal transduction.Understanding molecular mechanisms of disease resistance in plants willlead to the development of technology in enhancing plants' innate defenseto control infection. Such technology has the potential to reduce the useof hazardous pesticides without using non-plant genes. Therefore, thestudy of plant-microbe interactions is of interest to advancement of basicscience as well as to protection of the environment and improvement ofhuman life.

本研究的长期目标是利用拟南芥作为模型系统来确定导致系统性获得抗性（SAR）的信号事件。SAR是一种继发性病原体耐药性，可在局部感染后引起。SAR具有广谱性和持久性。通过遗传筛选，NPR1已被确定为SAR的关键正调控因子；NPR1基因突变体对sar1诱导无反应。NPR1编码一种具有重要功能的蛋白-蛋白相互作用结构域、BTB结构域和锚蛋白-重复结构域的新蛋白。最近的数据表明，NPR1的核定位对其功能至关重要。在细胞核中，NPR1可能影响bZIP转录因子的tga亚类和wrky转录因子的活性，这两种转录因子分别被认为是致病相关（PR）基因的转录激活因子和转录抑制因子。对npr1抑制因子的基因筛选导致了sni1的鉴定，这是一种恢复npr1中PR基因系统诱导的突变。野生型SNI1被认为是SAR的负调控因子，其失活需要NPR1的功能。假设npr1通过激活TGA转录激活因子和灭活wrky转录抑制因子来诱导SAR，并解除SNI1的负调控。在本项目中，分子遗传学和生化实验旨在(1)确定在SAR中，enpr1和WRKY转录因子相互作用的功能意义；(2)确定SNI1作为SAR负调节因子的作用机制；(3)鉴定npr1复合体中的成分。由于NPR1， SNI1和WRKY转录因子是新的或植物特异性的蛋白质，表征这些成分可能揭示新的信号转导机制。了解植物抗病的分子机制将有助于提高植物抗病技术的发展。这种技术有可能在不使用非植物基因的情况下减少有害农药的使用。因此，研究植物与微生物的相互作用不仅对促进基础科学的发展，而且对保护环境和改善人类生活具有重要意义。