Salicylic acid mediated protection of Brassica campestris sp. chinensis from saline stress via SA receptor NPR1 dependent transcriptional regulation and biosynthesis of related biochemicals

Salt stress has a significant impact on plant physiological processes and morphology, resulting in reduced plant performance. This study aimed to evaluate the hormonal regulation of Pakchoi ( Brassica campestris spp. chinensis) in response to saline stress imposition and exogenous salicylic acid application, focusing on morphological and physiological parameters. Saline stress imposition altered the concentration of endogenous hormonal levels, as demonstrated by Jasmonic acid (JA) and abscisic acid (ABA). Alterations in the level of plant hormones coincided with the enhanced reactive oxygen species (ROS) generation and proline accumulation followed by redox imbalances. Proline biosynthesis and antioxidative enzymes were significantly elevated with SA pretreatment. SA augmented stress responses are corroborated by the upregulation of SA signaling genes ( NPR1 and PR-1 ) and with a repressive effect on the expression of JA and ABA synthesis-related genes ( NCED3 , MYC2, PDF1.2 ). Moreover, the concerted action of SA-mediated genes might be associated with upregulation of flavonoid biosynthesis pathway genes ( FLS, CHS, CHI, F3H and ANS ), resulting in an enhanced level of phenolic compounds in SA pre-treated plants. A substantial scavenging property is attributed to phenolic compounds for the maintenance of cellular redox status. The results suggest that SA receptor NPR1 dependent transcriptional regulation and biosynthesis of related biochemicals are collaborative processes to counteract the adverse effects of salinity and maintain plant cellular redox homeostasis. • S.A pretreatment remediates saline stress induced symptoms. • Salicylic acid mediated modulation of endogenous hormones, as well as their signaling genes. • SA Receptor NPR1 dependent transcriptional regulation of biochemicals involves in redox control under saline stress.