MOLECULAR BASIS OF PATHOGEN INDUCED CELL DEATH IN PLANTS

病原体诱导植物细胞死亡的分子基础

• 批准号: 2715272
• 负责人: Jean T. Greenberg
• 金额: $ 11.77万
• 依托单位: UNIVERSITY OF CHICAGO
• 依托单位国家: 美国
• 财政年份: 1996
• 资助国家: 美国
• 起止时间: 1996-05-01 至 2001-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2715272
• 关键词: Arabidopsis; Pseudomonas; biological models; biological signal transduction; cell death; molecular cloning; pathologic process; plant diseases; plant genetics

DESCRIPTION: This proposal focuses on the mechanism of regulation and execution of a pathogen-triggered cell death program called the hypersensitive response (HR) in plants. The HR is part of a rapidly deployed defense response which functions to limit the spread of a pathogenic infection. Previously, a strategy was developed to study mechanism of HR control. The investigator isolated Arabidopsis plants which, due to single gene mutations, are able to bypass pathogen exposure to activate the HR and additional defenses. Plants harboring these mutations (called acd2 for accelerated cell death) show the HR, but harbor no infections agents. Since the acd2 mutations are recessive, the investigator's model is that ACD2 negatively regulates the HR and multiple defense functions. To understand the regulation and execution of the HR, the specific goals of this project are: to clone and characterize the ACD2 gene and its product, to identify the likely cell death inducing and regulatory genes under ACD2 control, and to identify additional genes that interact with ACD2 in the cell death regulatory pathway. Recent studies in the field of pathogenesis suggest that certain plant and animal pathogens have common pathogenicity genes. On the host side, both plant and animal cells can undergo programmed cell death during pathogen attack. The possibility exists that similar mechanisms of regulation and execution of cell death are used by both plants and animals. The ability to do genetics, molecular biology and biochemistry with both the pathogen and the host makes the study of host- pathogen interactions using the model system of Arabidopsis and Pseudomonas attractive for elucidating the mechanism and role of pathogen-induced cell death. In addition to activating the HR, the acd2 mutants activate at least two other defense pathways that are usually triggered only after certain pathogens infect wild-type plants. These pathways require two signals: the known signal molecule salicylic acid and an as yet uncharacterized signal. The long term goals of this work are to understand how these pathways are coordinately regulated by the ACD2-controlled signal(s), how the cell death program is activated and how the components of the signal transduction pathway(s) activate ACD2-controlled defenses.

描述：本提案重点关注监管机制和 执行病原体触发的细胞死亡程序，称为 植物的过敏反应（HR）。 人力资源部是快速发展的一部分 部署防御反应，其作用是限制病毒的传播 病原体感染。 此前，制定了一项策略来研究 人力资源控制机制。 研究人员分离出拟南芥植物 由于单基因突变，它们能够绕过病原体 暴露以激活心率和其他防御。 植物庇护 这些突变（称为 acd2，用于加速细胞死亡）显示 HR， 但不含有感染因子。 由于 acd2 突变是 隐性，研究者的模型是 ACD2 负向调节 人力资源和多种防御功能。 了解法规并 HR的执行，该项目的具体目标是：克隆 并表征 ACD2 基因及其产物，以确定可能的 ACD2 控制下的细胞死亡诱导和调节基因，以及 鉴定在细胞死亡过程中与 ACD2 相互作用的其他基因 监管途径。 发病机制领域的最新研究表明 某些植物和动物病原体具有共同的致病基因。 在宿主方面，植物和动物细胞都可以进行编程 病原体攻击期间细胞死亡。 存在类似的可能性 细胞死亡的调节和执行机制被两者使用 植物和动物。 遗传学、分子生物学和 病原体和宿主的生物化学使得宿主的研究 使用拟南芥模型系统和病原体相互作用 假单胞菌对于阐明其机制和作用具有吸引力 病原体诱导的细胞死亡。 除了激活HR之外，acd2突变体还激活至少两个 其他防御途径通常仅在某些特定条件后才会触发 病原体感染野生型植物。 这些途径需要两个信号： 已知的信号分子水杨酸和尚未表征的信号分子 信号。 这项工作的长期目标是了解这些 通路由 ACD2 控制的信号协调调节， 细胞死亡程序是如何被激活的以及细胞死亡程序的组成部分是如何 信号转导途径激活 ACD2 控制的防御。