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

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 HO is crucial to trigger stress response and enhance stress tolerance. However, the dynamic regulation mechanism of HO remains unclear. Here, we show that MhCAT2 (catalase 2 in Malus hupehensis) undergoes oxidative modification in an O-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 HO caused by salt stress-induced catalase (CAT) over-expression. Overall, this finding provides mechanistic insights on stress tolerance augmentation by an O-mediated switch that regulates HO homeostasis in Malus hupehensis.