Ricerc@Sapienza

In order to cause a disease, pathogens need to break the plant cell wall and to this purpose they secrete degrading enzymes towards various cell wall components. Several oligosaccharides released during pathogenesis, such as the Oligogalacturonides (OGs) and Cellodextrins (CDs) upon the breakdown of the homogalacturonan and cellulose respectively, act as Damage-Associated Molecular Patterns (DAMPs) and activate immunity. However, an over-accumulation of DAMPs may lead to a hyper-immunity characterized by a reduction of growth and, sometimes, cell death; for example, an over-accumulation of OGs leads to a hyper-immunity phenotype. Therefore, it is conceivable that the response to DAMPs must be controlled through homeostatic mechanisms to prevent hyper-immunity. We have discovered that four Arabidopsis Berberine Bridge Enzyme-like (BBE-like) proteins (OGOX1-4) oxidize OGs and impair their elicitor activity. We have also discovered another member of the BBE-like enzymes (CELLOX) which is expressed coordinately with OGOX1 during immunity and that specifically oxidizes CDs, also impairing their elicitor activity. Moreover, plants overexpressing OGOX1 or CELLOX display an enhanced resistance to Botrytis cinerea, likely because oxidized OGs and CDs are a less valuable carbon source for Botrytis. Thus, the capacity of impairing the activity of the cell wall-derived DAMPs is one important feature of BBE-like proteins that it may serve for the homeostatic control of the level of DAMPs.