Hydrogen sulfide - cysteine cycle system enhances cadmium tolerance through alleviating cadmium-induced oxidative stress and ion toxicity in Arabidopsis roots

Cadmium (Cd(2+)) is a common toxic heavy metal ion. We investigated the roles of hydrogen sulfide (H(2)S) and cysteine (Cys) in plant responses to Cd(2+) stress. The expression of H(2)S synthetic genes LCD and DES1 were induced by Cd(2+) within 3 h, and endogenous H(2)S was then rapidly released. H(2)S promoted the expression of Cys synthesis-related genes SAT1 and OASA1, which led to endogenous Cys accumulation. The H(2)S and Cys cycle system was stimulated by Cd(2+) stress, and it maintained high levels in plant cells. H(2)S inhibited the ROS burst by inducing alternative respiration capacity (AP) and antioxidase activity. H(2)S weakened Cd(2+) toxicity by inducing the metallothionein (MTs) genes expression. Cys promoted GSH accumulation and inhibited the ROS burst, and GSH induced the expression of phytochelatin (PCs) genes, counteracting Cd(2+) toxicity. In summary, the H(2)S and Cys cycle system played a key role in plant responses to Cd(2+) stress. The Cd(2+) tolerance was weakened when the cycle system was blocked in lcddes1-1 and oasa1 mutants. This paper is the first to describe the role of the H(2)S and Cys cycle system in Cd(2+) stress and to explore the relevant and specificity mechanisms of H(2)S and Cys in mediating Cd(2+) stress.