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

一个水稻拟病斑突变体（cv. Sekiguchi-asahi）对稻瘟病菌的抗性增强，从而诱导了光下Sekiguchi病斑（sl）的形成和色胺的积累。在有叶绿体的绿色组织中诱导自发的Sekiguchi病变，但在无叶绿体的白化病组织中不诱导。感染M.用光合作用抑制剂3-（3，4-二氯苯基）-1，1-二甲基脲（DCMU）预处理稻瘟病菌，可抑制色氨酸脱羧酶基因表达、单胺氧化酶活性、H_2O_2产生和DNA片段化。叶绿体似乎是sl突变体细胞死亡的关键介质。过氧化氢酶活性受M.而DCMU处理的叶片中则维持了较高的水平。光依赖性Sekiguchi病变的繁殖性质表明色胺介导的细胞死亡是由可扩散的试剂如过氧化氢引起的。此外，色氨酸在M.在光照条件下，DCMU处理对稻瘟病菌感染的叶片无明显影响。这种DCMU对色胺途径介导的细胞死亡的抑制在外源色氨酸存在下消失，表明光依赖性色胺积累和M.稻瘟病菌感染

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.