The Role of Nitric Oxide in Programmed Cell Death in Higher Plants

Abstract

Programmed cell death (PCD) is a genetically controlled biological process involved in defense, development, and stress response. Generally, the characters of plant PCD are similar to animal apoptosis, for instance cytoplasm shrinkage, chromatin condensation, and DNA fragmentation. An important signaling molecule, nitric oxide (NO) has been implicated in environmental-induced plant PCD, but its signaling and controlling network is still unknown. Whether NO promotes or suppresses PCD depends on NO sources and concentration in different plant species and environmental conditions. The effects of NO on developmental PCD were extensively studied. NO not only plays a crucial role in hypersensitive response (HR) during plant-pathogen interactions, but is also involved in abiotic stress-induced PCD including heat shock, salt, drought, cold, UV radiation, ozone, and heavy metals (mainly cadmium, aluminum). Previous studies showed the mitochondrion as a modulating center of PCD and also control NO level in planta. Vacuole processing enzyme (VPE) and caspase-like protein are involved in PCD. NO regulates the expression of PCD-associated genes via mitogen-activated protein kinase (MAPK) cascade, S-nitrosylation, and cGMP-dependent pathway. In addition, there are diverse interactions between NO and other signals such as hydrogen peroxide, calcium, ethylene, and salicylic acid (SA) during PCD. Based on understanding of related knowledge, NO signaling network in response to PCD in higher plants is presented in this chapter.