Increased tryptophan decarboxylase and monoamine oxidase activities induce Sekiguchi lesion formation in rice infected with Magnaporthe grisea.

Increased tryptophan decarboxylase and monoamine oxidase activities induce Sekiguchi lesion formation in rice infected with Magnaporthe grisea.
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DOI:
10.1046/j.1365-313x.2003.01875.x
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发表时间:
2003-10
期刊:
The Plant journal : for cell and molecular biology
影响因子:
--
通讯作者:
M. Ueno;H. Shibata;J. Kihara;Y. Honda;S. Arase
M. Ueno;H. Shibata;J. Kihara;Y. Honda;S. Arase
中科院分区:
其他
文献类型:
--
作者:
M. Ueno;H. Shibata;J. Kihara;Y. Honda;S. Arase

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关口病斑(sl)突变体水稻感染稻瘟病菌后,光依赖性色氨酸脱羧酶(TDC)和单胺氧化酶(MAO)活性显著升高。在M.稻瘟病菌对水稻细胞的影响,即使在Sekiguchi病斑形成后也保持高水平。TDC基因在接种M.在关口病斑形成之前对稻瘟病菌的致病性进行研究。M.稻瘟病菌还诱导了Sekiguchi病斑的形成,伴随着酶活性的增加和色胺的积累。关口损伤也诱导色胺和β-苯乙胺,这是底物的单胺氧化酶,但不诱导非底物,如吲哚-3-丙酸,(+/-)-苯乙胺和色氨酸在光下。在MAO抑制剂甲霜灵和氨基脲以及H2O2清除剂抗坏血酸和过氧化氢酶的存在下,色胺对Sekiguchi病变的光依赖性诱导被显著抑制。H2O2在M.通过强3,3'-二氨基联苯胺(DAB)染色直接原位显示了带有和不带有Sekiguchi损伤的稻瘟病菌感染的叶片。另一方面,H_2O_2诱导黄瓜叶片上的Sekiguchi病变。关口朝日在光下,但不是在黑暗中。这种差异与光下感染叶片中过氧化氢酶活性的降低和黑暗中没有降低有关。我们推测H_2O_2诱导的叶肉细胞中叶绿体和线粒体等细胞器的破坏可能导致TDC和MAO活性的升高和Sekiguchi病斑的发生,野生型水稻中的sl基因产物可能对化学或环境胁迫引起的细胞器破坏起抑制作用。
Sekiguchi lesion (sl)-mutant rice infected with Magnaporthe grisea showed increased light-dependent tryptophan decarboxylase (TDC) and monoamine oxidase (MAO) activities. TDC and MAO 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 (SGF) of M. grisea also induced Sekiguchi lesion formation accompanied by increased enzymes activities and tryptamine accumulation. Sekiguchi lesion was also induced by treatments with tryptamine and beta-phenylethylamine, which are substrates for MAO, but was not induced by non-substrates such as indole-3-propionic acid, (+/-)-phenylethylamine and tryptophan under light. Light-dependent induction of Sekiguchi lesion by tryptamine was significantly inhibited in the presence of MAO inhibitors, metalaxyl and semicarbazide, and H2O2-scavengers, ascorbic acid and catalase. H2O2 in M. grisea-infected leaves with and without Sekiguchi lesions was demonstrated directly in situ by strong 3,3'-diaminobenzidine (DAB) staining. On the other hand, H2O2 induced Sekiguchi lesions on leaves of cv. Sekiguchi-asahi under light, but not in darkness. This difference was associated with the decrease of catalase activity in infected leaves under light and the absence of decrease in darkness. We hypothesize that the H2O2-induced breakdown of cellular organelles such as chloroplasts and mitochondria in mesophyll cells may cause high TDC and MAO activities and the development of Sekiguchi lesion, and that the sl gene products in wild-type rice may function as a suppressor of organelle breakdown caused by chemical or environmental stress.