The Role of Growth Regulators in Senescence

Abstract The inevitable, genetically programmed process of senescence, which is basically a series of actions focusing on the disintegration in cellular structures and the carriage of materials released in the process, is regulated by many factors, both internal and external. The internal factors involved—namely, plant growth regulators (PGRs), reactive oxygen species (ROS), and the carbon/nitrogen (C/N) relationship—produce signals that can accelerate or delay senescence. PGRs stand as important components that influence leaf senescence either by regulating when it begins and how it progresses or by inducing deferent responses to internal and external signals (which include abiotic and biotic factors). The transcriptome profiles of stress responses and leaf senescence indicate that significant cross-talk exists among these processes. Genes expressed in young, photosynthetic-active leaves are downregulated during senescence, and at the same time senescence-associated genes (SAGs) are upregulated. This in turn means that SAG expression is responsible for senescence and thus is the target for hormonal regulation. PGRs such as ethylene, jasmonic acid (JA), brassinosteroids (BRs), salicylic acid (SA), and abscisic acid (ABA) play a significant role in inducing leaf senescence, while gibberellic acid (GA), cytokinins (CKs), polyamines, and auxin may suppress leaf senescence. SA, JA, ethylene, and ABA are also known to be greatly involved in various abiotic and biotic stress responses, which affect the synthesis and signaling pathways of the hormones to eventually trigger the expression of stress-responsive genes, which in turn appears to affect leaf senescence. Although the process of senescence occurs in the whole plant, leaf, root, and flower, this chapter will focus on leaf senescence and how it can be regulated by PGRs.