Mild drought priming-induced salicylic acid involves in subsequent drought tolerance by modulating glutathione redox in antagonism with abscisic acid in Brassica napus

Abstract

This study aimed to characterize the drought priming effects on the interactive regulation of oxidative burst signaling and hormones in the glutathione (GSH) pathway and GSH-based redox control during the subsequent drought period. Plants were exposed to mild drought for 7 days, re-watered for 12 days, and subjected to subsequent drought stress for 18 days. Mild drought stress-responsive increase in salicylic acid (SA) level and signaling was more prominent compared to those of abscisic acid (ABA), leading to an increase in GSH level. During the subsequent drought period, drought-induced reactive oxygen species (ROS) accumulation and lipid peroxidation were significantly reduced in mild drought-primed plants, resulting in a depression of oxidative burst-inducible gene 1 (OXI1). The ABA level and the expression of ABA synthesis genes, 9-sis-epoxycarotenoid dioxygenase 3 (NCED3) and ABA-responsive element binding protein 2 (AREB2), predominantly enhanced in non-primed plants, while they depressed distinctly with an antagonistic enhancement of SA level and SA-responsive genes, isochorismate synthase1 (ICS1) and non-expression of the pathogenesis-related gene1 (NPR1), in mild drought-primed plants. Drought-responsive loss of reducing potential in GSH-based redox was positively recovered with up-regulation of genes encoding glutathione synthetase 1 (GSH1) and glutathione reductase 1 (GR1) as well as redox-related genes (thioredoxin-h5 [TRXh5] and CC-type glutaredoxin 9 [GRXC9]). The present results support that the priming with mild drought effectively functions in alleviating subsequent severe drought stress, as evidenced by less wilting with better-maintaining leaf water potential and less loss of photosynthetic pigments, by activating SA-mediated modulation of the GSH pathway and GSH redox control in antagonism with ABA responses. © 2023, The Author(s), under exclusive licence to Springer Nature B.V.