The hypersensitive response and its role in local and systemic disease resistance
2001
Kombrink, E. | Schmelzer, E.
A ubiquitous feature of plant/pathogen interactions is host cell death that is manifested as rapid collapse of tissue and is termed the hypersensitive response (HR). This response accompanies many but not all incompatible interactions and is considered one of the important mechanisms leading to resistance. The sites of HR, the infection sites proper, are invariably the focal points for transcriptional activation of a large variety of plant defence genes in neighbouring cells. The subsequent biosynthesis of protective secondary metabolites and inhibitory proteins around the infection sites are considered to be important for overall pathogen containment. In addition, local HR is often associated with the onset of systemic acquired resistance (SAR) in distal plant tissues. This type of resistance is generally effective against a broad range of pathogens and it is associated with the transcriptional activation of whole set of marker genes, many of which encode pathogenesis-related proteins, such as chitinases and 1,3-beta-glucanases. Cell death is also a feature of disease symptoms in many compatible interactions, but in these cases it usually occurs rather late during the course of host colonisation by the pathogen. Necrotic lesions may develop but are not required for triggering SAR and systemic gene activation. Apparently, different forms of cell death and mechanisms leading to HR exist and are executed in plant/pathogen interactions. Although the importance of small molecules, such as reactive oxygen intermediates (ROI), for the establishment of HR cell death has been recognized, a functional and causal link between ROI production, initiation of HR cell death, and induced local and systemic disease resistance remains to be unequivocally demonstrated.
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