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Reactive oxygen species produced by NADPH oxidase regulate plant cell growth

机译:NADPH氧化酶产生的活性氧调节植物细胞的生长

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Cell expansion is a central process in plant morphogenesis, and the elongation of roots and root hairs is essential for uptake of minerals and water from the soil. Ca2+ influx from the extracellular store is required for ( and sets the rates of) cell elongation in roots(1). Arabidopsis thaliana rhd2 mutants are defective in Ca2+ uptake and consequently cell expansion is compromised rhd2 mutants have short root hairs(2,3) and stunted roots. To determine the regulation of Ca2+ acquisition in growing root cells we show here that RHD2 is an NADPH oxidase, a protein that transfers electrons from NADPH to an electron acceptor leading to the formation of reactive oxygen species (ROS). We show that ROS accumulate in growing wild-type (WT) root hairs but their levels are markedly decreased in rhd2 mutants. Blocking the activity of the NADPH oxidase with diphenylene iodonium (DPI) inhibits ROS formation and phenocopies Rhd2(-). Treatment of rhd2 roots with ROS partly suppresses the mutant phenotype and stimulates the activity of plasma membrane hyperpolarization-activated Ca2+ channels, the predominant root Ca2+ acquisition system. This indicates that NADPH oxidases control development by making ROS that regulate plant cell expansion through the activation of Ca2+ channels. [References: 29]
机译:细胞膨胀是植物形态发生的核心过程,根和根毛的伸长对于从土壤中吸收矿物质和水分至关重要。 Ca2 +从细胞外储入是根部细胞伸长所必需的(并确定其速率)(1)。拟南芥rhd2突变体在Ca2 +吸收方面存在缺陷,因此细胞扩增受到损害。rhd2突变体的根毛短(2,3)和根部发育不良。为了确定生长中的根细胞中Ca2 +获取的调控,我们在这里显示RHD2是NADPH氧化酶,一种将电子从NADPH转移到电子受体的蛋白质,导致形成活性氧(ROS)。我们显示,ROS在生长的野生型(WT)根毛中积累,但它们的水平在rhd2突变体中明显降低。用二亚苯基碘鎓(DPI)阻断NADPH氧化酶的活性可抑制ROS的形成和表型Rhd2(-)。用ROS处理rhd2根部分抑制了突变表型并刺激了质膜超极化激活的Ca2 +通道(主要的根Ca2 +采集系统)的活性。这表明NADPH氧化酶通过使ROS通过Ca2 +通道的活化来调节植物细胞的膨胀来控制发育。 [参考:29]

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