Cross Talk between Reactive Nitrogen and Oxygen Species during the Hypersensitive Disease Resistance Response

Abstract

In recent years, nitric oxide (NO) has been identified as a fundamental molecule that interplays with reactive oxygen species (ROS) in a variety of ways, either as a crucial partner in determining cell fate or in signaling in response to a number of physiological and stress-related conditions. The best characterized relationship between NO with ROS refers to its role in plant defense against pathogen attack, in particular in the establishment of the hypersensitive reaction (HR; Wendehenne et al., 2004; Delledonne, 2005). HR is a form of programmed cell death that contributes to plant resistance by restricting the invading pathogen at the infection site and shows some regulatory and mechanistic features characteristic of apoptosis in animal cells, like membrane dysfunction, vacuolization of the cytoplasm, chromatin condensation, and endonucleolytic cleavage of DNA (Greenberg and Yao, 2004). Activation of the HR triggers a number of rapid cellular responses, including perturbations of ion fluxes and changes in the pattern of protein phosphorylation (Lamb and Dixon, 1997), which precede the accumulation of ROS and NO. The oxidative and nitrosative bursts are then followed by a signal cascade that mediates transcriptional activation of defense genes and finally the local and systemic expression of antimicrobial proteins, leading to the establishment of systemic acquired resistance (McDowell and Dangl, 2000).