The 2012 ASHS Annual Conference

The production of reactive oxygen species (ROS) is one of the earliest cellular responses which mediating defense gene activation following successful pathogen recognition. The amount of extracellular H₂O₂ is produced depends on several factors including the nature of the elicitor, the plant species, and age or developmental stages of the plant cells. Several enzymes have been implicated in apoplastic ROS generation following pathogen recognition, i.e., reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, super oxide dismutase, oxalate oxidases, peroxidases, lipoxygenases and amine oxidases. ROS usually correlates with successful disease resistance responses however some pathogens may induce production of ROS to their own advantage. There are profound differences between monocots and dicots as well as in the biology of biotrophic, hemibiotrophic and necrotrophic pathogens. ROS acts synergistically in a signal amplification to drive the hypersensitive reaction (HR) and the establishment of systemic defenses. The role of ROS in successful pathogenesis, it is important to try to inhibit the cell death machinery selectively and simultaneously to monitor other defense and pathogenesis-related events. Avirulent pathogens successfully recognized via the action of disease resistance (R) gene products in plant immune system. However, virulent pathogens that avoid host recognition induce only the transient, low-amplitude first phase of this response, suggesting a role for ROS in the establishment of the defenses. Elicitors of defense responses, referred to as microbe or pathogen-associated molecular patterns (PAMPs), also trigger an oxidative burst. With the understanding of the molecular mechanisms underlying the localized activation of the oxidative burst following perception of pathogen avirulence signals and key downstream responses including gene activation, cell death, and long-distance signaling, novel strategies will be developed for engineering enhanced protection against pathogens by manipulation of the oxidative burst and oxidant-mediated signal pathways.