Role of Nitric Oxide in Plant Senescence

Abstract

In plants senescence is the final stage of plant growth and development that ultimately leads to death. Plants experience age-related as well as stress-induced developmental ageing. Senescence involves significant changes at the transcriptional, post-translational and metabolomic levels. Furthermore, phytohormones also play a critical role in the programmed senescence of plants. Nitric oxide (NO) is a gaseous signalling molecule that regulates a plethora of physiological processes in plants. Its role in the control of ageing and senescence has just started to be elucidated. Here, we review the role of NO in the regulation of programmed cell death, seed ageing, fruit ripening and senescence. We also discuss the role of NO in the modulation of phytohormones during senescence and the significance of NO-ROS cross-talk during programmed cell death and senescence.

Keywords: ROS; ageing; nitric oxide; programmed cell death; senescence.

Figure 1

Role of nitric oxide in fruit ripening, programmed cell death and leaf senescence. (A) NO and ROS-mediated control of programmed cell death. Plants rapidly-produce NO and various ROS in response to biotic and/or abiotic stresses leading to intrinsic execution of the target cells. NO and ROS can trigger PCD either synergistically or independently. Both NO and ROS are implicated in the hypersensitive response (HR), characterized by the execution of the infected and surrounding cells, is a well-known form of PCD in plants. However, significant cross-talk exists between NO and ROS during the establishment of HR. The establishment of HR warrants a critical balance between intracellular levels of NO and ROS. Several key proteins such as non-expressor of pathogensi-related genes 1 (NPR1), TGA1 (transcriptional activators that specifically bind to 5′-TGACG-3′), glyceraldehyde-3-phosphate dehydrorgenase (GAPDH), respiratory burst oxidase homolog D (RBOHD) are involved in HR are known to be S-nitrosated by NO or affected by the NO-ROS cross talk. NO is also known to scavenge H₂O₂ under certain circumstances thereby protecting plant cells from ROS-mediated damage. (B) NO-mediated regulation of senescence, seed dormancy and fruit ripening. NO affects leaf senescence by modulating phytohormones such as ABA, ET, and JA. Though the role of NO in seed ageing is not well-defined, NO is known to break seed dormancy via stimulation of ET production. NO donors and arginine (Arg) abolishes seed dormancy and stimulates germination whereas, the application of NO scavengers (such as cPTIO, L-Name, and CAN) promotes seed dormancy. NO-mediated removal of seed dormancy and promotion of germination is associated with alternations of nitrated and biotinylated proteins, ABA, JA and protein nitration. NO has also been implicated in fruit ripening. As the fruit ripens, ROS and RNS anabolic vs. catabolic rates change significantly altering the overall nitro-oxidative environment at the cellular level ultimately affecting the NO-dependent S-Nitorsation and Tyrosine Nitration events in fruit. Furthermore, NO mediated binding and chelation, S-nitrosylation of methionine adenosyl transferase (MAT), stoichiometric reduction of ACC and transcriptional regulation of several genes involved in the ethylene pathway plays an important role in fruit ripening.