Abstract

Salinity-alkalinity stress is a limiting environmental factor in muskmelon production. Treatment with γ-aminobutyric acid (GABA) protects crops against several abiotic stresses. Previous studies reported that GABA increased the content of polyamines (PAs) and improved the oxidative stress tolerance of muskmelon grown under salinity-alkalinity stress. However, it was unclear whether PAs were involved in GABA-regulated salinity-alkalinity stress tolerance. Here, we explored the roles of PAs in GABA-regulated Na+/K+ homeostasis and membrane lipid peroxidation. Our results showed that GABA pretreatment reduced the salinity-alkalinity stress-induced inhibition of muskmelon growth, significantly reduced the Na+/K+ ratio and enhanced the contents of free PAs, arginine, and methionine. GABA treatment upregulated the expression levels of PA-related genes under salinity-alkalinity stress. Application of exogenous spermidine reduced the salinity-alkalinity stress-induced inhibition of muskmelon growth, relative electrical conductivity, malondialdehyde content, and Na+/K+ ratio. By contrast, pretreatment of muskmelon plants with the Spd synthesis inhibitor dicyclohexylammonium sulfate (DCHA) eliminated GABA-remediated ion balance, membrane peroxidation injury, and plant growth under salinity-alkalinity stress conditions. In all, fed with GABA maintained the Na+/K+ balance via reducing Na+ content and increasing K+ uptake of muskmelon under salinity-alkalinity stress conditions, ultimately reduced membrane oxidation injury. And GABA provoked PAs levels involved in GABA-regulated Na+/K+ homeostasis and alleviation of membrane lipid peroxidation under salinity-alkalinity stress tolerance.

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