Molecular Mechanisms for Regulating Programmed Cell Death during Host-Pamsite Interactions

1.使用燕麦无细胞系统对植物细胞凋亡进行分子剖析宿主特异性毒素维克托灵诱导敏感燕麦品种的细胞凋亡。为了研究植物细胞凋亡的发生机制，我们建立了一个燕麦无细胞凋亡系统。燕麦组织的细胞提取物经Victorin诱导的细胞凋亡引起细胞核塌陷和核小体间DNA片段化。药理学研究表明，半胱氨酸蛋白酶对E-64敏感，但对半胱氨酸蛋白酶特异性抑制剂不敏感，是细胞核形态变化的重要组成部分，核酸酶和半胱氨酸蛋白酶协同作用诱导细胞凋亡DNA梯状化。有趣的是，这一发现与那些在充分研究的动物无细胞系统中的发现形成对比，其中凋亡核酸内切酶单独负责DNA片段化。植物过敏反应诱导和抑制的分子机制 关于我们 马铃薯晚疫病菌（Phytophthora infestans）的蛋白质激发子（INF] elicitin）、马铃薯假单胞菌（Pseudomonasseiningae）的harpin和鞭毛蛋白（flagellin）诱导过敏性细胞死亡。对导致过敏反应（HR）的信号转导途径的药理学研究表明，HR需要从头蛋白质合成和蛋白质磷酸化。鞭毛蛋白是一种新发现的HR诱导子，其HR活性受翻译后糖基化修饰的调控。我们还鉴定了新的防御反应相关的植物基因，并表征了它们的结构，表达和功能。OPR基因是植物中一个重要的基因，在亲和互作中被特异诱导。OPR可能参与了植物防御反应的抑制.寄主特异性毒素ACR毒素的作用方式粗柠檬和真菌病原体互交链格孢菌粗柠檬致病型之间相互作用的特异性由寄主选择性毒素ACR毒素决定。ACR-毒素的靶位点是线粒体DNA，称为ACRS（ACR-毒素敏感性基因），负责毒素敏感性。我们确定了对ACR毒素的敏感性/或不敏感性以及因此互作的特异性。互作的粗柠檬致病型和宿主植物之间的相互作用是由于ACRS的差异转录后加工。少

1. Molecular dissection of plant apoptosis using an oat cell free systemThe host specific toxin, victorin induces apoptotic cell death in sensitive oat cultivars. We have developed an oat cell-free apoptosis system to investigate the execution mechanisms of plant apoptosis. Cell extracts derived from oat tissues undergoing victorin-induced apoptosis caused nuclear collapse and internucleosomal DNA fragmentation in isolated nuclei Pharmacological studies revealed that cysteine pretense, which is E-64-sensitive but insensitive to caspase-specific inhibitors, is a crucial component in the morphological change of isolated nuclei, and that nuclease and the cysteine protease act cooperatively to induce the apoptotic DNA laddering. Interestingly, this finding is contrasted with those in well-studied animal cell-free systems in which an apoptotic endonuclease is solely responsible for the DNA fragmentation.2. Molecular mechanisms of induction and suppression of plant hypersensitive response tr … More iggered by proteinaccous elicitors INF] elicitin from Phytophthora infestans, harpin and flagellin from Pseudomonas syringae induce hypersensitive cell death. Pharmacological investigation of the signal transduction pathway leading to hypersensitive response (HR) revealed that HR requires de novo protein synthesis and protein phosphorylation. Flagellin is a newly identified HR elicitor, and its HR activity is regulated by post-translational glicosyl-modification. We also identified novel defense response-related plant genes, and characterized their structure, expression and function. One of the interesting plant genes, OPR is found to be induced specifically in compatible interactions. OPR may be involved in the suppression of plant defense response.3. The mode of action of the host specific toxin, ACR toxinSpecificity in the interaction between rough lemon and the fungal pathogen Alternaria alternate rough lemon pathotype is determined by a host-selective toxin, ACR-toxin. The target site of ACR-toxin is mitochondrion, and mitochondrial DNA sequence, designated ACRS (ACR-toxin Sensitivity gene), is responsible for the toxin sensitivity. We identified that sensitivity/or insensitivity to ACR-toxin and hence specificity of the interaction between the A.alternata rough lemon pathotype and host plants is due to differential post-transcriptional processing of ACRS. Less