Oxidative post-translational modification of catalase confers salt stress acclimatization by regulating H2O2 homeostasis in Malus hupehensis

Abstract

Reactive oxygen species (ROS) play an essential role as both signaling molecule and damage agent during salt stress. As a signaling molecule, proper accumulation of H₂O₂ is crucial to trigger stress response and enhance stress tolerance. However, the dynamic regulation mechanism of H₂O₂ remains unclear. Here, we show that MhCAT2 (catalase 2 in Malus hupehensis) undergoes oxidative modification in an O₂^•--dependent manner and that oxidation at His225 residue reduces the MhCAT2 activity. Furthermore, the substitution of His225 with Tyr weakens the activity of MhCAT2. The oxidation modification provides a post-translational brake mechanism for the excessive scavenging of H₂O₂ caused by salt stress-induced catalase (CAT) over-expression. Overall, this finding provides mechanistic insights on stress tolerance augmentation by an O₂^•--mediated switch that regulates H₂O₂ homeostasis in Malus hupehensis.