A CC-Type Glutaredoxins GRX480 Functions in Cadmium Tolerance by Maintaining Redox Homeostasis in Arabidopsis

• Published in: International journal of molecular sciences Vol. 25; no. 21; p. 11455
• Main Authors: Li, Ying-Rui, Cai, Wei, Zhang, Ya-Xuan, Zhang, Ning-Xin, Huang, Qiao-Ling, Lu, Ying-Tang, Yuan, Ting-Ting
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 01-11-2024; MDPI
• Subjects: Antioxidants; Arabidopsis thaliana; Cadmium; Chlorophyll; Enzymes; Genetic transcription; Homeostasis; Oxidative stress; Plant growth; Proline; Proteins; Thiols; Toxicity; China
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms252111455

Cadmium (Cd) toxicity causes oxidative stress damage in plant cells. Glutaredoxins (GRXs), a type of small oxidoreductase, play a crucial role in modulating thiol redox states. However, whether GRXs act in Cd stress remains to be identified. Here, we reveal that Arabidopsis GRX480, a member of the CC-type family, enhances plant Cd stress tolerance. The GRX480 mutants exhibit enhanced sensitivity to Cd stress, manifested by shortened root, reduced biomass, lower chlorophyll and proline levels, and decreased photosynthetic efficiency compared with the wild type. The Cd concentration in GRX480 mutants is higher than the wild type, resulting from the inhibition of Cd efflux and transport genes transcription. Lower levels of GSH were detected in Cd-treated GRX480 mutants than in the wild type, indicating that GRX480 regulates plant Cd tolerance by influencing the balance between GSH and GSSG. Furthermore, the hyperaccumulation of reactive oxygen species (ROS) is associated with decreased expression of H2O2 scavenging genes in Cd-treated GRX480 mutants. Additionally, more toxic reactive carbonyl species (RCS), produced during oxidative stress, accumulate in Cd-treated GRX480 mutants than in wild type. Overall, our study establishes a critical role of GRX480 in response to Cd stress, highlighting its multifaceted contributions to detoxification and the maintenance of redox homeostasis.