An increase of methyl-esterification of pectin reduces the susceptibility of plants to fungal and bacterial infection

The plant cell wall is a physical barrier against pathogens and its modification is often associated to changes in plant defense responses. Pectin is responsible for mechanical properties of the wall such as porosity, adhesion and rigidity and is the substrate of pectin-degrading enzymes such polygalacturonases (PG) and pectin methylesterases (PME). The action of these enzymes is the pre-requisite for subsequent cell wall degradation by other polysaccharidedegrading enzymes. Pectin is synthesized in a highly methylesterified form and is subsequently de-esterified in muro by PME. On the other hand PME activity is finely regulated by the presence of multiple enzyme isoforms and by the action of pectin-metylesterase inhibitors (PMEI). PME knockout and PMEI over-expression have been used to stably increase pectin methylesterification in Arabidopsis plants. We will present results showing that decrease of PME activity and associated increase of pectin methylesterification are correlated to a decreased susceptibility of Arabidopsis to Pectobacterium carotovorum and Botrytis cinerea.