Nitric oxide acts upstream of indole-3-acetic acid in ameliorating arsenate stress in tomato seedlings

Abstract

After their discovery, nitric oxide (NO) and indole-3-acetic acid (IAA) have been reported as game-changing cellular messengers for reducing abiotic stresses in plants. But, information regarding their shared signaling in regulating metal stress is still unclear. Herein, we have investigated about the joint role of NO and IAA in mitigation of arsenate [As(V)] toxicity in tomato seedlings. Arsenate being a toxic metalloid increases the NPQ level and cell death while decreasing the biomass accumulation, photosynthetic pigments, chlorophyll a fluorescence, endogenous NO content in tomato seedlings. However, application of IAA or SNP to the As(V) stressed seedlings improved growth together with less accumulation of arsenic and thus, preventing cell death. Interestingly, addition of c-PTIO, {2-(4-carboxyphenyl)-4, 4, 5, 5-tetramethylimidazoline-1-oxyl-3-oxide, a scavenger of NO} and 2, 3, 5-triidobenzoic acid (TIBA, an inhibitor of polar auxin transport) further increased cell death and inhibited activity of GST, leading to As(V) toxicity. However, addition of IAA to SNP and TIBA treated seedlings reversed the effect of TIBA resulting into decreased As(V) toxicity. These findings demonstrate that IAA plays a crucial and advantageous function in NO-mediated reduction of As(V) toxicity in seedlings of tomato. Overall, this study concluded that IAA might be acting as a downstream signal for NO-mediated reduction of As(V) toxicity in tomato seedlings.