Abiotic stress-triggered oxidative challenges: Where does H2S act?

Hydrogen sulfide (H2S) was once principally considered the perpetrator of plant growth cessation and cell death. However, this has become an antiquated view, with cumulative evidence showing that the H2S serves as a biological signaling molecule notably involved in abiotic stress response and adaptation, such as defense by phytohormone activation, stomatal movement, gene reprogramming, and plant growth modulation. Reactive oxygen species (ROS)-dependent oxidative stress is involved in these responses. Remarkably, an ever-growing body of evidence indicates that H2S can directly interact with ROS processing systems in a redox-dependent manner, while it has been gradually recognized that H2S-based posttranslational modifications of key protein cysteine residues determine stress responses. Furthermore, the reciprocal interplay between H2S and nitric oxide (NO) in regulating oxidative stress has significant importance. The interaction of H2S with NO and ROS during acclimation to abiotic stress may vary from synergism to antagonism. However, the molecular pathways and factors involved remain to be identified. This review not only aims to provide updated information on H2S action in regulating ROS-dependent redox homeostasis and signaling, but also discusses the mechanisms of H2S-dependent regulation in the context of oxidative stress elicited by environmental cues. Copyright (C) 2022, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, and Genetics Society of China. Published by Elsevier Limited and Science Press. All rights reserved.