Biochemical mechanisms regulating salt tolerance in sunflower

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Abstract
Sunflower plants are semi-tolerant to salt stress. Calcium modulates the expression of oubain-sensitive ATPases, responsible for sodium fluxes in cells. Salt stress delays degradation of oil body (OB) membrane proteins. Serotonin and melatonin contents are elevated in response to salt stress. Melatonin can detoxify the seedlings of elevated reactive oxygen species (ROS) levels. Enhanced nitric oxide (NO) expression correlates with NaCl-induced modulation of seedling growth. Salt stress enhances S-nitrosylation of cytosolic proteins in seedling cotyledons, while in roots, denitrosylation of proteins is observed. Lipid peroxide content and glutathione peroxidase (GPX4) activity are enhanced in response to salt stress. Salt stress downregulates the activity of superoxide dismutase (SOD) and upregulates the activity of GPX4 and glutathione reductase (GR). Heme oxygenase-1 (HO-1) abundance in cells surrounding the secretory canal in seedling cotyledons is enhanced in response to salt stress. NO negatively regulates the total glutathione homeostasis and regulates polyamine and glycine betaine homeostasis in response to salt stress. An intricate biochemical crosstalk is thus observed to control salt tolerance mechanisms in sunflower.