Glutathione-mediated regulation of nitric oxide, S-nitrosothiol and redox homeostasis confers cadmium tolerance by inducing transcription factors and stress response genes in tomato
Glutathione-mediated regulation of nitric oxide, S-nitrosothiol and redox homeostasis confers cadmium tolerance by inducing transcription factors and stress response genes in tomato
复制标题
谷胱甘肽介导的一氧化氮、S-亚硝基硫醇和氧化还原稳态的调节通过诱导番茄转录因子和应激反应基因赋予镉耐受性
DOI：
10.1016/j.chemosphere.2016.07.053
复制
发表时间：
2016-10-01
期刊：
影响因子：
8.8
通讯作者：
Xia, Xiao-Jian
中科院分区：
文献类型：
--
作者：
Hasan, Md. Kamrul;Liu, Congcong;Xia, Xiao-Jian
谷胱甘肽（GSH）在植物生长发育和逆境应答中起着重要作用。然而，GSH调节镉（Cd）胁迫耐受性的机制仍不清楚。在这里，我们表明，谷胱甘肽生物合成的抑制丁硫氨酸亚砜（BSO）加重镉的毒性，增加积累的活性氧（ROS）和减少一氧化氮（NO）和S-亚硝基硫醇（SNO）在番茄根。与此相反，外源GSH缓解镉毒性大大减少ROS积累和增加NO和SNO的含量，和抗氧化酶的活性，最终降低氧化应激。GSH诱导的镉耐受性增强与几种转录因子如乙烯反应性转录因子1（ERF 1）、ERF 2、MYB 1转录因子-AIM 1和R2 R3-MYB转录因子-AN 2以及一些应激反应基因的转录上调密切相关。此外，GSH通过维持GSH：GSSG和阿萨：DHA比值的增加来调节细胞的氧化还原平衡，并增加植物螯合素的含量。尽管如此，GSH诱导的缓解镉的植物毒性也与增加螯合镉进入细胞壁和液泡，但不与镉积累。在Cd胁迫下，BSO处理略有降低Cd的液泡分数，而BSO和GSH联合处理则显著增加了该分数。我们的研究结果表明，GSH增加番茄耐镉胁迫不仅通过促进螯合和螯合镉，但也通过刺激NO，SNO和抗氧化系统通过氧化还原依赖性机制。(C)2016爱思唯尔有限公司版权所有
Glutathione (GSH) plays a critical role in plant growth, development and responses to stress. However, the mechanism by which GSH regulates tolerance to cadmium (Cd) stress still remains unclear. Here we show that inhibition of GSH biosynthesis by buthionine sulfoximine (BSO) aggravated Cd toxicity by increasing accumulation of reactive oxygen species (ROS) and reducing contents of nitric oxide (NO) and S-nitrosothiol (SNO) in tomato roots. In contrast, exogenous GSH alleviated Cd toxicity by substantially minimizing ROS accumulation and increasing contents of NO and SNO, and activities of antioxidant enzymes that eventually reduced oxidative stress. GSH-induced enhancement in Cd tolerance was closely associated with the upregulation of transcripts of several transcription factors such as ETHYLENE RESPONSIVE TRANSCRIPTION FACTOR 1 (ERF1), ERF2, MYB1 TRANSCRIPTION FACTOR- AIM1 and R2R3-MYB TRANSCRIPTION FACTOR- AN2, and some stress response genes. In addition, GSH modulated the cellular redox balance through maintaining increased GSH: GSSG and AsA: DHA ratios, and also increased phytochelatins contents. Nonetheless, GSH-induced alleviation of Cd phytotoxicity was also associated with increased sequestration of Cd into cell walls and vacuoles but not with Cd accumulation. Under Cd stress, while treatment with BSO slightly decreased vacuolar fraction of Cd, combined treatment with BSO and GSH noticeably increased that fraction. Our results suggest that GSH increases tomato tolerance to Cd stress not only by promoting the chelation and sequestration of Cd but also by stimulating NO, SNO and the antioxidant system through a redox-dependent mechanism. (C) 2016 Elsevier Ltd. All rights reserved.