Glutathione-mediated regulation of nitric oxide, S-nitrosothiol and redox homeostasis confers cadmium tolerance by inducing transcription factors and stress response genes in tomato. (October 2016)

• Record Type: Journal Article
• Authors: Hasan, Md. Kamrul; Liu, Congcong; Wang, Fanan; Ahammed, Golam Jalal; Zhou, Jie; Xu, Ming-Xing; Yu, Jing-Quan; Xia, Xiao-Jian
• Is Part Of: Chemosphere. Volume 161(2016)
• Page Start: 536
• Page End: 545
• Publication Date: 2016-10
• Subjects: Cadmium -- Glutathione -- Nitric oxide -- Phytochelatin -- Tomato -- Vacuolar sequestration; Pollution -- Periodicals; Pollution -- Physiological effect -- Periodicals; Environmental sciences -- Periodicals; Atmospheric chemistry -- Periodicals; 551.511
• DOI: 10.1016/j.chemosphere.2016.07.053
• Languages: English
• ISSNs: 0045-6535

Abstract

Abstract: 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. Highlights: GSH enhanced production of NO and total S -nitrosothiol contents under Cd stress. GSH maintained a reduced cellular redox status and increased antioxidant capacity. GSH induced transcripts of transcription factors and antioxidant genes. GSH increased PCs content by inducing transcription of PCS. GSH prompted the sequestration of Cd into the cell walls and vacuoles.