Molecular Basis of Pathogen-Induced Cell Death in Plants

这一竞争更新概述了将模式植物拟南芥强大的分子遗传学与细胞生物学方法相结合的实验，以检查与病程相关的程序性细胞死亡(PCD)调节和执行中涉及的几个关键基因的功能。了解PCD的控制对于制定控制PCD的策略以预防或治愈涉及PCD诱导过多或不足的疾病非常重要。PCD在植物中被称为“过敏性反应”(HR)，有助于限制某些病原体的传播和/或增强其他防御。植物有第二个较慢的PCD反应，称为敏感细胞死亡，促进病原体的生长和传播，并由不导致HR的病原体触发。这两种类型的PCD都受到基因控制，在某些情况下都需要一种名为水杨酸(SA)的共同信号分子。然而，启动HR以响应某些病原体并不需要SA。这些意见提出了重要的问题，即PCD的管理和/或执行是否由多个独立的机制进行，或者是否有一些核心步骤。为了解决这些问题，并阐明与HR和易感细胞死亡相关的PCD控制所需的步骤，我们鉴定了几个与细胞死亡和防御调节有关的基因，称为加速细胞死亡(ACD)。这项拟议的研究涉及细胞死亡和抗病途径中一种新的依赖SA的信号成分ACD6的作用机制，对依赖SA的ACD5基因在疾病期间对细胞死亡至关重要的特征，以及确定一种SA不依赖的机制，在结构上与PCD诱导的动物原卟啉IX相关的叶绿素分解代谢在疾病期间诱导细胞死亡。研究计划的一个更开放的方面是通过使用基因筛查来识别额外的基因，这些基因对于疾病和HR期间发生的细胞死亡的积极和消极调节非常重要。最后，一个重要的目标是利用ACD和其他突变体发展细胞生物学检测，以直接可视化和研究单个死亡细胞的特性和信号需求，并确定线粒体和/或叶绿体参与协调PCD。

This competing renewal outlines experiments that combine the powerful molecular genetics of the model plant Arabidopsis with cell biological approaches to examine the function of several key genes involved in pathogenesis-associated programmed cell death (PCD) regulation and execution. Understanding the control of PCD is important for developing strategies to manipulate PCD to prevent or cure diseases involving excess or insufficient PCD induction. Known in plants as the "hypersensitive response" (HR), PCD aids in limiting the spread of some pathogens and/or amplifying other defenses. Plants have a second, slower PCD response, called susceptible cell death, that facilitates pathogen growth and transmission and is triggered by pathogens that do not cause an HR. Both types of PCD are subject to genetic control and in some cases both require a common signaling molecule called salicylic acid (SA). However, initiation of the HR in response to some pathogens does not require SA. These observations have raised important questions as to whether the regulation and/or execution of PCD occurs by multiple independent mechanisms or whether there are some core steps. To address these questions and to elucidate the steps required for the control of PCD associated with the HR and susceptible cell death, several genes termed ACCELERATED CELL DEATH (ACD) important for cell death and defense regulation were identified. The proposed research addresses the mechanism of action of a novel SA-dependent signaling component of the cell death and disease resistance pathway called ACD6, the characterization of the SA-dependent ACD5 gene important for cell death during disease and the determination an SA-independent mechanism whereby chlorophyll catabolites, structurally related to the PCD-inducing protoporphyrin IX in animals, induce cell death during disease. A more open ended aspect of the research program is the identification of additional genes, through the employment of genetic screens, important for the positive and negative regulation of cell death that occurs during disease and the HR. Finally, an important goal is to exploit the acd and other mutants in the development of cell biological assays to directly visualize and study the properties and signaling requirements of single dying cells and to determine the involvement of mitochondria and/or chloroplasts in coordinating PCD.