MOLECULAR BASIS OF PATHOGEN INDUCED CELL DEATH IN PLANTS

说明：本提案侧重于监管机制， 执行一个病原体触发的细胞死亡程序， 过敏反应（HR）。 HR是一个快速的 部署防御反应，其作用是限制病毒的传播 病原体感染 此前，制定了一项战略， HR控制机制。 研究者分离出拟南芥植物 由于单基因突变， 暴露以激活人力资源和额外的防御。 庇护植物 这些突变（称为acd 2表示细胞加速死亡）显示HR， 但不含有感染因子。 由于acd 2突变是 隐性的，研究者的模型是ACD 2负调节 人力资源和多种防御功能。 了解法规， 人力资源的执行，这个项目的具体目标是：克隆 并描述ACD 2基因及其产物，以确定可能的 ACD 2控制下的细胞死亡诱导和调节基因，以及 鉴定在细胞死亡中与ACD 2相互作用的其他基因 调控途径 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， 病原体攻击时细胞死亡 有可能类似的 细胞死亡的调节和执行机制被两者所使用。 植物和动物 有能力做遗传学，分子生物学和 生物化学与病原体和宿主一起研究宿主- 病原体的相互作用使用的模式系统拟南芥和 假单胞菌的吸引力，阐明机制和作用， 病原体诱导的细胞死亡。 除了激活HR之外，acd 2突变体还激活至少两个 其他防御途径通常只在某些情况下才会被触发， 病原体感染野生型植物。 这些通路需要两个信号： 已知信号分子水杨酸和一种尚未表征的 信号了 这项工作的长期目标是了解这些 途径由ACD 2控制的信号协调调节， 细胞死亡程序是如何被激活的， 信号转导途径激活ACD 2控制防御。

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.