Spatial regulation of NADPH oxidase RBOHD for ROS production during salt stress response

Abstract

Various environmental stresses can induce production of ROS to turn on signaling for proper responses to those stresses. Plasma membrane (PM)-localized RBOHs, in particular RBOHD, produce ROS via the posttranslational activation upon abiotic and biotic stresses. Although the mechanisms of RBOHD activation upon biotic stress have been elucidated in detail, it remains elusive how salinity stress activates RBOHD. Here, I present evidence that trafficking of PM-localized RBOHD to endosomes and then its recycling back to the PM is critical for ROS accumulation upon salinity stress. ateca4 plants that were defective in recycling of proteins from endosomes to the PM and clc2-1 and chc2-1 plants that were defective in endocytosis showed a defect in salinity stress-induced ROS production. In addition, ateca4 plants showed a defect in transient accumulation of GFP:RBOHD to the PM at the early stage of salinity stress. By contrast, ateca4 plants showed no defect in the increase in the ROS level and accumulation of RBOHD to the PM upon flg22 treatment as wild-type plants. Based on these observations, I propose that trafficking machinery such as AtECA4 and clathrin are important players for salt stress-induced, but not flg22-induced, ROS accumulation.