ABSTRACT
Cold stress positively modulates nitric oxide (NO) production via various enzymatic pathways [Nitric oxide synthase like (NOS-like), nitrate reductase (NR)] and non-enzymatic pathways (reduction of nitrite). Enhanced NO contributes to SNO accumulation which causes the oxidation of the SH group in proteins leading to S-nitrosylation, a post-translational modification (PTM) of NO. Major cold responsive S-nitrosylated proteins belong to stress/signaling/redox, photosynthesis, metabolism and cell wall modification, showing the regulation of major cellular metabolic pathways by S-nitrosylation. Among S-nitrosylated targets, 33% showed more than one NO-based PTM, suggesting the existence of PTM cross-talk in cold stress. NO positively modulates the activity of antioxidant enzymes, superoxide dismutase (SOD), catalase (CA), peroxidase (POD), ascorbate peroxidase (APX), monodehydroascorbate reductase (MDHAR) and dehydroascorbate reductase (DHAR), causing detoxification of ROS generated in cold stress. Denitrosylation is also a crucial mechanism of stress tolerance in plants. Another interesting development is the discovery of putative receptors for NO. NO is able to induce stress acclimation response prior to stress, making it a strong candidate for priming. This chapter highlights recent advancements in NO signaling during cold stress for the understanding of the cross-talk mechanisms.
