Molecular elucidation of hypersensitive cell death in lesion mimic mutants of rice infected with Magnaporthe grisea.

色氨酸脱羧酶（TDC）和单胺氧化酶（MAO）活性升高。在稻瘟病菌侵入水稻细胞之前观察到这些酶的活性，即使在关口病形成后也保持高水平。在稻瘟病形成前，在接种了稻瘟病菌的叶片中观察到TDC基因的光依赖性表达。稻瘟病菌孢子萌发液也能诱导关口病的形成，并伴有酶活性和色胺积累的增加。在光照条件下，以MAO为底物的处理也能诱导Sekiguchi病变，而非底物处理在光照条件下无诱导作用。在MAO抑制剂和h_2o_2清除剂存在的情况下，色胺对关口病变的光依赖性诱导被显著抑制。在经环己亚胺（CHX）或高温（HS）处理过的Sekiguchi病变突变体叶片中，Sekiguchi病变的形成和稻瘟病菌侵染后色胺的积累均明显受到抑制。在CHX或hs预处理的叶片中，TDC和MAO活性的光依赖性诱导也被显著抑制。光照条件下，稻瘟病菌接种后的关口病突变体叶片DNA片段化和DNA酶活性显著提高。然而，在CHX或hs预处理的叶片中，即使在光照下也没有观察到阶梯状和dna酶活性。末端脱氧核苷酸转移酶介导的dUTP-nic末端标记染色和凝胶分析表明，关口病叶片组织细胞存在DNA断裂。这些数据表明：1)长波长光激活关口病突变体的色胺途径，2)长波长光照射（550 ~ 650nm）抑制了稻瘟病菌接种的关口病突变体过氧化氢酶活性，并通过H_2O_2的产生和积累激活了色胺途径，3)关口病突变体的形成是一种类似凋亡的反应，其反应是由光依赖性的色胺途径激活引起的。这是增强抗光性的原因。少

Increased tryptohan decarboxylase(TDC) and monoamine oxidase(MAO) activities were observed in Sekiguchi lesion mutant infected with Mgrisea. These enzyme activities were observed before the penetration of M. grisea to rice cells and maintained high levels even after Sekiguchi lesion formation. Light-dependent expression of TDC gene was observed in leaves inoculated with M.grisea before Sekiguchi lesion formation. Spore germination fluid of M grisea also induced Sekiguchi lesion formation accompanied by increased enzymes activities and tryptamine accumulation. Sekiguchi lesion was also induced by treatments with substrates for MAO under light, but not induced by non-substrates under light. Light-dependent induction of Sekiguchi lesion by tryptamine was significantly inhibited in the presence of MAO inhibitors and H_2O_2-scavengers. In cycloheximide(CHX)- or heat (HS)-pre-treated leaves of the Sekiguchi lesion mutant, the formation of Sekiguchi lesions and the accumulation of tryptamine … More by M.grisea infection were significantly inhibited. In the CHX- or HS-pre-treated leaves, light-dependent induction of both TDC and MAO activities was also significantly inhibited. DNA fragmentation and DNase activity were significantly induced in leaves of the Sekiguchi lesion mutant inoculated with M.grisea under light. In the CHX- or HS-pre-treated leaves, however, neither laddering nor DNase activity was observed even under light. Terminal deoxynucleotidyl transferase-mediated dUTP-nic end labeling staining and gel analysis indicated DNA fragmentation in cells of leaf tissues with Sekiguchi lesions.These data show that : 1)Tryptamine pathway in the Sekiguchi lesion mutants is activated by light of long wavelength, 2)Catalase activity is inhibited by light irradiation of long wavelengths (550-650nm) in sekiguchi lesion mutant inoculated with M. grisea, and tryptamine pathway was activated by H_2O_2 generation and accumulation, 3)Sekiguchi lesion formation in the Sekiguchi lesion mutants is an apoptosis-like response and that its response is induced by light-dependent activation of the tryptamine pathway, which is responsible for light-enhanced resistance. Less