Nitric oxide mediates γ-aminobutyric acid-enhanced muskmelon tolerance to salinity–alkalinity stress conditions

Abstract

Salinity–alkalinity stress severely limits muskmelon production. γ-Aminobutyric acid (GABA) is a free amino acid that enhances crop resistance to environmental stresses. Nitric oxide (NO) is associated with numerous physiological processes and an important signal molecule in plant response to stress. However, whether NO plays roles in GABA-improved salinity–alkalinity tolerance of muskmelon is unclear. Here, we used exogenous sodium nitroprusside (SNP, NO donor) or 2- (4- carboxyphenyl)- 4,4,5,5-tetramethylimidazoline-1- oxyl-3-oxide (cPTIO, a NO scavenger) or GABA to investigate whether NO mediates GABA-induced muskmelon salinity–alkalinity tolerance by regulating antioxidation and Na+/K+ homeostasis to maintain cell membrane stability/integrity. Salinity–alkalinity stress could induce the NO production, and GABA pretreatment also increased NO content, nitrate reductase activity, and NO synthase activity under salinity–alkalinity conditions. Exogenous SNP could increase the activities of antioxidase and mitigate salinity–alkalinity stress inhibited plant growth and decreased the malondialdehyde content, relative electrical conductivity and Na+/K+ ratio in muskmelon. By contrast, pretreatment of plants subjected to salinity–alkalinity stress with cPTIO abolished the GABA-enhanced plant growth and antioxidation, remediation of membrane peroxidation damage, and restoration of ion balance; but no significant effects on endogenous GABA levels. Thus, NO may act as a downstream signal of GABA to stimulate the antioxidant system which then regulate membrane lipid peroxidation and ion homeostasis, and ultimately increase the salinity–alkalinity stress tolerance of muskmelon and promote the plant growth.