Nitric Oxide and Reactive Oxygen Species in PCD Signaling

Abstract

Abstract Programmed cell death (PCD) is a process of genetically encoded and actively controlled cellular suicide. PCD is associated with different phases of plant life and also represents a defence mechanism that plants activate against different kinds of biotic and abiotic stresses. Reactive oxygen species (ROS) and nitric oxide (NO) have been proposed as key factors in the control of both developmentally and environmentally induced PCD. In this chapter, we give an overview of ROS and NO interplay in the signaling leading to PCD induced in senescence, self-incompatibility, hypersensitive response and under cadmium and heat stress. The data presented indicate that ROS and NO interact through different pathways, depending on the level and the timing of production of these reactive species, the cellular redox state and the plant species. Despite the complicate network of signals, some common points of NO/ROS crosstalk in the different kinds of PCD can be identified. First, during PCD, ROS and NO biosynthesis is mutually regulated with feedback mechanisms. The NO-dependent S-nitrosylation of proteins controlling ROS levels represents a key point of interaction of the two species. Furthermore, NO and ROS interplay could amplify the induction of PCD executors, such as caspase-3-like. Finally, NO and/or ROS might control the ubiquitin–proteasome pathway involved in PCD induction.