Nitric Oxide Contributes to Cadmium Toxicity in Arabidopsis by Promoting Cadmium Accumulation in Roots and by Up-Regulating Genes Related to Iron Uptake
Nitric Oxide Contributes to Cadmium Toxicity in Arabidopsis by Promoting Cadmium Accumulation in Roots and by Up-Regulating Genes Related to Iron Uptake
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DOI：
10.1104/pp.108.133348
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发表时间：
2009-03-01
期刊：
影响因子：
7.4
通讯作者：
Wendehenne, David
中科院分区：
文献类型：
--
作者：
Besson-Bard, Angelique;Gravot, Antoine;Wendehenne, David
一氧化氮（NO）是植物体内的一种细胞信号分子。特别是，NO在铁稳态的调节和植物对有毒金属的反应中的作用已被提出。在这里，我们调查的合成和NO的作用在植物暴露于镉（Cd 2+），一种非必需的和有毒的金属。我们证明，镉诱导拟南芥（拟南芥）幼苗的根和叶中NO的合成。这种生产，这是敏感的NO合成酶抑制剂，不涉及硝酸还原酶和AtNOA 1，但需要IRT 1，编码一个主要的质膜转运铁，但也镉2+。通过分析Cd 2+处理过程中NO清除或抑制其合成的发生率，我们证明了NO有助于Cd 2+引发的根系生长抑制。为了了解这一过程的机制，进行了微阵列分析，以确定NO-调制的根基因的上调和下调Cd 2+处理。43个基因被确定编码与铁稳态，蛋白水解，氮同化/代谢，根生长相关的蛋白质。这些基因包括IRT 1。调查的金属和离子含量在Cd 2+处理的根中，NO合成受损表明，IRT 1上调NO的一致相关NO的能力，以促进Cd 2+在根中的积累。这一分析还强调，NO是负责Cd 2+诱导的抑制根Cd 2+积累。两者合计，我们的研究结果表明，NO有助于Cd 2+的毒性有利于Cd 2+与Cd 2+的吸收，并通过启动类似的细胞途径激活后，铁剥夺。
Nitric oxide (NO) functions as a cell-signaling molecule in plants. In particular, a role for NO in the regulation of iron homeostasis and in the plant response to toxic metals has been proposed. Here, we investigated the synthesis and the role of NO in plants exposed to cadmium (Cd2+), a nonessential and toxic metal. We demonstrate that Cd2+ induces NO synthesis in roots and leaves of Arabidopsis (Arabidopsis thaliana) seedlings. This production, which is sensitive to NO synthase inhibitors, does not involve nitrate reductase and AtNOA1 but requires IRT1, encoding a major plasma membrane transporter for iron but also Cd2+. By analyzing the incidence of NO scavenging or inhibition of its synthesis during Cd2+ treatment, we demonstrated that NO contributes to Cd2+-triggered inhibition of root growth. To understand the mechanisms underlying this process, a microarray analysis was performed in order to identify NO-modulated root genes up-and down-regulated during Cd2+ treatment. Forty-three genes were identified encoding proteins related to iron homeostasis, proteolysis, nitrogen assimilation/metabolism, and root growth. These genes include IRT1. Investigation of the metal and ion contents in Cd2+-treated roots in which NO synthesis was impaired indicates that IRT1 up-regulation by NO was consistently correlated to NO's ability to promote Cd2+ accumulation in roots. This analysis also highlights that NO is responsible for Cd2+-induced inhibition of root Cd2+ accumulation. Taken together, our results suggest that NO contributes to Cd2+ toxicity by favoring Cd2+ versus Cd2+ uptake and by initiating a cellular pathway resembling those activated upon iron deprivation.