Abstract
Plants have evolved several mechanisms to prevent invasion of their tissues by pathogens. A common feature of disease resistance is the hypersensitive response at and immediately surrounding infection sites, which is characterized by the formation of necrotic lesions. Following to this local resistance response, tissue distal to the infection site develops a systemic acquired resistance to a secondary infection by the same or by different pathogens. During the hypersensitive response, massive accumulation of H2O2 from the oxidative burst functions as a diffusible signal for the induction of cellular protectant genes, mediates a systemic signal network in the establishment of plant immunity and is required, but not sufficient, to trigger localized host cell death. Nitric oxide, a well known host-defense component in animal systems, co-operates with reactive oxygen intermediates in the induction of hypersensitive cell death, and functions independently of such intermediates in the induction of defense related genes.KeywordsNitric OxideNitric OxideSalicylic AcidHypersensitive ResponseOxidative BurstThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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