Hydrogen sulfide maintains redox homeostasis and suppresses ganoderic acids biosynthesis under heat stress via S-sulfhydrating thioredoxin 1 in Ganoderma lucidum

Abstract

Abstract Hydrogen sulfide (H2S) is considered to be a novel gaseous signalling molecule with multiple physiological functions. Recently, the identification of sulfhydrated proteins has become a new hotspot in the analysis of the underlying mechanism of H2S. Our preliminary study has shown that H2S negatively regulates the heat-induced accumulation of ganoderic acids (GAs)，a major secondary metabolite in Ganoderma lucidum. However, a comprehensive understanding of its mechanism is lacking. In this study, sulfhydrated proteins in G. lucidum were quantified by quantitative proteomic mass spectrometry (MS), and the role of H2S in maintaining redox homeostasis under heat stress (HS) was determined. A redox-regulated protein, thioredoxin 1 (Trx1), was selected as a potential target of H2S. Further research revealed that the activity of Trx1 was provoked by sulfhydration at Cys31 and Cys34, contributing to the negative regulation of H2S to ROS accumulation and GAs biosynthesis under HS in G. lucidum. Our results provide a novel target for investigating the molecular mechanism of H2S physiological function. Moreover, new evidence is provided regarding the interaction mechanism between the H2S and ROS signalling pathways.