Calcium signalling inhibition disrupts nitric oxide-mediated regulation of reactive oxygen species (ROS), antioxidant defense, photosynthesis, nitrate reductase, proline metabolism, and SOS/NIA expression, compromising salinity stress tolerance in Brassica juncea L.
摘要
Salinity stress upsets redox balance and causes an accumulation of excess reactive oxygen species, which hinders plant growth and product yield. This study explores the role of calcium ions (Ca2⁺) as a crucial downstream mediator of nitric oxide (NO) downstream signalling in Brassica juncea under salinity stress. A detailed physiological and biochemical study showed that exogenous treatment of NO and Ca2⁺ alleviated salinity-induced damage by increasing the antioxidant defense system, ALAD activity, photosynthetic efficiency, and water use efficiency by 40% compared to salinity (p < 0.05), and maintaining proline homeostasis. However, the joint treatment of NO and calcium ion inhibitors (EGTA and LaCl3) exacerbated stress symptoms, suggesting the importance of Ca2⁺ in NO-induced stress tolerance. To gain insight into the mechanisms, the transcriptional profiling of salt-responsive genes was carried out. The data showed that treatment of NO and Ca2⁺ greatly induced the expression of SOS1, SOS2, SOS3, NIA1, and NIA2 genes, suggesting that ion homeostasis and nitrate assimilation were enhanced. On the contrary, the Ca2⁺ signalling pathway inhibitor greatly inhibited expression of these genes, suggesting that Ca2⁺ played a crucial role in the NO-induced gene expression. Cumulatively, this study highlights the complementary function of NO and Ca2⁺ in regulating stress-responsive physiological properties and transcriptional networks. The results of this study provide important information on the molecular mechanisms involved in plant response and adaptation under stress conditions and provide a potential strategy for improving salinity tolerance in Brassica juncea.