Glutathione (GSH) is an essential redox buffer in the response to biotic and abiotic stresses. Unfavourable environmental conditions induce the production of reactive oxygen species (ROS) and other oxidized compounds in the cell, which needs to be controlled to avoid oxidative damage. Moreover, the redox state of GSH constitutes an important molecular marker in plant defence responses, which can be modulated by stress-related signaling molecules like salicylic acid (SA).
This work aimed to validate, in an in vivo system, the role of SA in modulating the GSH redox state under oxidative stress, and to evaluate if genes with antioxidant functions induced by SA may be responsible for the antioxidant effect mediated by this hormone. To establish an optimized methodology for monitoring in real-time the redox state of GSH under different stress conditions, we used the GRX1-roGFP2 redox sensor.
SA-deficient genotypes confirmed the importance of this hormone in the redox control of GSH under UV and MeV treatments. Furthermore, this investigation shed light on the role of GSTU7 in the tolerance to methyl viologen (MeV). GSTU7 is a SA-induced gene that codes for an antioxidant enzyme with GSH-dependent functions. Our work indicates that GSTU7 expression is required for the contention of MeV-induced oxidative damage, reducing ROS production and maintaining a more reduced GSH redox state.
These results suggest GSTU7 as one of the genes responsible for the antioxidant activity in response to stress.