Besson-Bard Angélique, Gravot Antoine, Richaud Pierre, Auroy Pascaline, Duc Céline, Gaymard Frédéric, Taconnat Ludivine, Renou Jean-Pierre, Pugin Alain, Wendehenne David
UMR INRA 1088/CNRS 5184/Université de Bourgogne, Plante-Microbe-Environnement, 21065 Dijon cedex, France.
Plant Physiol. 2009 Mar;149(3):1302-15. doi: 10.1104/pp.108.133348. Epub 2009 Jan 23.
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 (Cd(2+)), a nonessential and toxic metal. We demonstrate that Cd(2+) 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 Cd(2+). By analyzing the incidence of NO scavenging or inhibition of its synthesis during Cd(2+) treatment, we demonstrated that NO contributes to Cd(2+)-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 Cd(2+) 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 Cd(2+)-treated roots in which NO synthesis was impaired indicates that IRT1 up-regulation by NO was consistently correlated to NO's ability to promote Cd(2+) accumulation in roots. This analysis also highlights that NO is responsible for Cd(2+)-induced inhibition of root Ca(2+) accumulation. Taken together, our results suggest that NO contributes to Cd(2+) toxicity by favoring Cd(2+) versus Ca(2+) uptake and by initiating a cellular pathway resembling those activated upon iron deprivation.
一氧化氮（NO）在植物中作为一种细胞信号分子发挥作用。特别地，有人提出NO在铁稳态调节以及植物对有毒金属的响应中发挥作用。在此，我们研究了暴露于镉（Cd²⁺）（一种非必需的有毒金属）的植物中NO的合成及其作用。我们证明Cd²⁺诱导拟南芥（Arabidopsis thaliana）幼苗根和叶中NO的合成。这种对NO合酶抑制剂敏感的产生不涉及硝酸还原酶和AtNOA1，但需要IRT1，IRT1编码一种主要的质膜铁转运蛋白，同时也转运Cd²⁺。通过分析在Cd²⁺处理期间NO清除或其合成抑制的发生率，我们证明NO有助于Cd²⁺触发的根生长抑制。为了理解这一过程的潜在机制，进行了微阵列分析以鉴定在Cd²⁺处理期间上调和下调的NO调节的根基因。鉴定出43个编码与铁稳态、蛋白水解、氮同化/代谢和根生长相关蛋白质的基因。这些基因包括IRT1。对NO合成受损的Cd²⁺处理根中的金属和离子含量进行研究表明，NO对IRT1的上调与NO促进根中Cd²⁺积累的能力一致相关。该分析还突出表明NO是Cd²⁺诱导的根Ca²⁺积累抑制的原因。综上所述，我们的结果表明NO通过促进Cd²⁺相对于Ca²⁺的吸收以及启动类似于铁缺乏时激活的细胞途径来促成Cd²⁺毒性。
