Molecular elucidation of tryptamine-pathway mediated hypersensitive cell death in lesion mimic mutants of rice infected with Magnaporthe grisea

感染稻瘟病菌的水稻病变模拟突变体中色胺途径介导的过敏性细胞死亡的分子阐明

基本信息

批准号：
17580039
负责人：
ARASE Sakae
金额：
$ 2.3万
依托单位：
Shimane University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

项目摘要

A lesion-mimic mutant of rice (cv. Sekiguchi-asahi) showed enhanced resistance to Magnaporthe grisea infection, thereby inducing Sekiguchi lesion (sl) formation and tryptamine accumulation under light. Spontaneous Sekiguchi lesions were induced in green tissues with chloroplasts, but not in albino tissues without chloroplasts. Both Sekiguchi lesion formation and tryptamine accumulation in leaves infected with M. grisea were inhibited by pre-treatment with the photosynthetic inhibitor, 3-(3,4-dicchlorophenyl)-1,1-dimethylurea (DCMU), which suppressed the gene expression of tryptophan decarboxylase, monoamine oxidase activity, H_2O_2 generation and DNA fragmentation. Chloroplasts appear to be the key mediators of cell death in the sl mutant. Catalase activity was significantly inhibited by M. grisea infection under light, but maintained a high level in leaves pretreated with DCMU. The propagative nature of light-dependent Sekiguchi lesions suggests that tryptamine-mediated cell death is caused by a diffusible agent such as hydrogen peroxide. Furthermore, tryptophan accumulated in M. grisea-infected leaves under light, but not in DCMU-pretreated ones. Such DCMU inhibition of tryptamine pathway-mediated cell death disappeared in the presence of exogenous tryptophan, suggesting a strong correlation between light-dependent tryptamine accumulation and the activation of the tryptophan biosynthetic pathway after M. grisea infection.

水稻的病斑模拟突变体（cv. Sekiguchi-asahi）表现出对稻瘟病菌感染的增强抵抗力，从而在光下诱导 Sekiguchi 病斑（sl）形成和色胺积累。自发性关口损伤是在有叶绿体的绿色组织中诱导的，但在没有叶绿体的白化组织中则不然。用光合抑制剂 3-(3,4-二氯苯基)-1,1-二甲基脲 (DCMU) 进行预处理，可抑制感染稻瘟病菌叶片中关口病斑的形成和色胺积累，从而抑制色氨酸脱羧酶、单胺氧化酶活性、H_2O_2 生成和 DNA 片段化。叶绿体似乎是 sl 突变体细胞死亡的关键介质。光下的稻瘟病菌感染显着抑制过氧化氢酶活性，但在用 DCMU 预处理的叶子中保持高水平。光依赖性关口病变的增殖性质表明色胺介导的细胞死亡是由过氧化氢等扩散剂引起的。此外，在光照下，色氨酸在稻瘟病菌感染的叶子中积累，但在经 DCMU 预处理的叶子中却没有积累。这种 DCMU 对色胺途径介导的细胞死亡的抑制作用在外源色氨酸存在的情况下消失，表明光依赖性色胺积累与稻瘟病菌感染后色氨酸生物合成途径的激活之间存在很强的相关性。