Regulatory mechanisms of ROI generation are affected by rice spl mutations
Regulatory mechanisms of ROI generation are affected by rice spl mutations
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DOI：
10.1093/pcp/pcj074
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发表时间：
2006-08-01
影响因子：
4.9
通讯作者：
Iba, Koh
中科院分区：
文献类型：
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作者：
Kojo, Kaori;Yaeno, Takashi;Iba, Koh
活性氧中间体（reactive oxygen intermediates，ROI）在植物抗病过程中的过敏反应（hypersensitive response，HR）中起着关键作用。NADPH氧化酶是ROI的主要来源;然而，其调节机制尚不清楚。水稻spl突变体自发形成的病变，类似于那些发生在HR，这表明突变影响的调节HR. We发现，spl 2，spl 7和spl 11突变体细胞积累了大量的H2 O2响应稻瘟病真菌激发子。增加的ROI的积累被抑制NADPH氧化酶的抑制在spl细胞中，也观察到在臭氧暴露的spl植物。与野生型相比，这些突变体具有足够的ROI清除酶活性。此外，spl 7突变体细胞积累了较高量的H2 O2时，用calyculin A（CA），蛋白磷酸酶抑制剂处理。此外，spl 2突变体植物表现出加速积累的H2 O2和增加的细胞死亡率响应于创伤。这些结果表明，spl 2，spl 7和spl 11突变体是在NADPH氧化酶的调节缺陷，spl 7突变可能会引起蛋白脱磷酸化控制的信号通路的增强，而spl 2突变影响病原体诱导和创伤诱导的信号通路。
Reactive oxygen intermediates (ROIs) play a pivotal role in the hypersensitive response (HR) in disease resistance. NADPH oxidase is a major source of ROI; however, the mechanisms of its regulation are unclear. Rice spl mutants spontaneously form lesions which resemble those occurring during the HR, suggesting that the mutations affect regulation of the HR. We found that spl2, spl7 and spl11 mutant cells accumulated increased amounts of H2O2 in response to rice blast fungal elicitor. Increased accumulation of ROIs was suppressed by inhibition of NADPH oxidase in the spl cells, and was also observed in the ozone-exposed spl plants. These mutants have sufficient activities of ROI-scavenging enzymes compared with the wild type. In addition, spl7 mutant cells accumulated higher amounts Of H2O2 when treated with calyculin A (CA), an inhibitor of protein phosphatase. Furthermore, spl2 mutant plants exhibited accelerated accumulation of H2O2 and increased rates of cell death in response to wounding. These results suggest that the spl2, spl7 and spl11 mutants are defective in the regulation of NADPH oxidase, and the spl7 mutation may give rise to enhancement of the signaling pathway which protein dephosphorylation controls, while the spl2 mutation affects both the pathogen-induced and wound-induced signaling pathways.