Abstract：
Cadmium (Cd), as a non-essential and toxic heavy metal in plants, has deleterious effects on plant physiological and biochemical processes. Nitric oxide (NO) is one of the most important signaling molecules for plants to response diverse stresses. Here, we found that Cd-induced programmed cell death (PCD) was accompanied by NO bursts, which exacerbated cell death when NO was removed and vice versa. Proteomic analysis of S-nitrosylated proteins showed that the differential proteins in Cd-induced PCD and in NO-alleviated PCD mainly exist together in carbohydrate metabolism and amino acid metabolism, while some of the differential proteins exist alone in metabolism of cofactors and vitamins and lipid metabolism. Meanwhile, S-nitrosylation of proteins in porphyrin and chlorophyll metabolism and starch and sucrose metabolism could explain the leaf chlorosis induced by PCD. Moreover, protein transport protein SEC23, ubiquitinyl hydrolase 1 and pathogenesis-related protein 1 were identified to be S-nitrosylated in vivo, and their expressions were increased in Cd-induced PCD while decreased in NO treatment. Similar results were obtained in tomato seedlings with higher S-nitrosylation. Taken together, our results indicate that NO might be involved in the regulation of Cd-induced PCD through protein S-nitrosylation, especially proteins involved in PCD response.
摘要：
镉(Cd),作为植物中的一种非必需和有毒的重金属，对植物生理和生化过程有有害影响。一氧化氮（NO）是植物响应多种胁迫的最重要的信号分子之一。这里,我们发现Cd诱导的程序性细胞死亡（PCD）伴随着NO爆发，当NO被去除时，这会加剧细胞死亡，反之亦然。S-亚硝基化蛋白质的蛋白质组学分析表明，Cd诱导的PCD和NO缓解的PCD中的差异蛋白主要存在于碳水化合物代谢和氨基酸代谢中。而一些差异蛋白单独存在于辅因子和维生素的代谢和脂类代谢中。同时,卟啉和叶绿素代谢以及淀粉和蔗糖代谢中蛋白质的S-亚硝基化可以解释PCD诱导的叶片萎黄病。此外，蛋白质转运蛋白SEC23，泛素酰水解酶1和发病相关蛋白1在体内被鉴定为S-亚硝基化，在Cd诱导的PCD中它们的表达增加，而在NO处理中它们的表达减少。在具有较高S-亚硝基化的番茄幼苗中获得了类似的结果。一起来看,我们的结果表明，NO可能通过蛋白质S-亚硝基化参与Cd诱导的PCD的调节，尤其是参与PCD反应的蛋白质。
