Active Oxygen Species in Plant Defense against Pathogens

TLDR

Plant disease resistance relies on early pathogen recognition that triggers a hypersensitive response (HR), causing localized necrosis and the release of toxic molecules to limit pathogen spread. The HR induces synthesis of antimicrobial phytoalexins, hydrolytic enzymes, and alterations in cell‑wall structural proteins.

Abstract

Plant disease resistance to pathogens such as fungi, bacteria, and viruses often depends on whether the plant is able to recognize the pathogen early in the infection process. The recognition event leads to a rapid tissue necrosis at the site of infection, which is called the HR. The HR deprives the pathogen of nutrients and/or releases toxic molecules, thereby confining pathogen growth to a small region of the plant. This response provides resistance to the great majority of potential pathogens (nonhost or species resistance). For a given plant species, a much more limited number of true pathogens exhibit the ability to evade the host recognition system and grow extensively within the plant without evoking host necrosis at a11 or only after considerable delay. In this case, the plant exhibits susceptibility and the extensive growth of the successful pathogen can cause varying degrees of damage. However, certain races within pathogenic bacteria1 or funga1 species are recognized by certain cultivars or genotypes of the host plant species and the HR is triggered. These observations indicate that there is an ongqing evolution of the host plant's ability to recognize pathogen races that were previously unrecognized while the pathogen evolves to avoid recognition by a previously resistant host. Recognition of pathogens triggers a large range of inducible defense mechanisms that are believed to contribute to overall resistance in the plant. The mechanisms induced at the site of infection and associated with the HR include synthesis of antimicrobial compounds called phytoalexins, synthesis of hydrolytic enzymes that attack fungi and bacteria, and alterations in the synthesis of cell-wall structural proteins (for