Host pectin methylesterase plays a role in the susceptibility to necrotrophic pathogens

The host cell wall is a primary target during growth of necrotrophic pathogens. During the first stages of infection, pectin, one of the main components of the plant cell wall, is degraded by pectinolytic enzymes produced by the majority of fungal and bacterial pathogens. Some evidence indicates that variation of the pectin structure and composition may cause an altered disease response upon infection with pathogens. Pectin is synthesized and secreted into the cell wall in a highly methylesterified form and, soon thereafter, deesterified in muro by pectin methylesterases (PMEs). The action of PME makes pectin susceptible to degradation by enzymes such as endo-polygalacturonases (PGs) and pectate lyases (PELs). Endogenous PME activity is controlled through the interaction with the pectin methylesterase inhibitor (PMEI). PMEI over-expression and PME knockout have been used to stably increase pectin methylesterification in Arabidopsis plants. We have shown that the increase of pectin methylesterification and the lack of a specific PME activity correlate to a decreased susceptibility of Arabidopsis to the necrotrophic pathogens Pectobacterium carotovorum and Botrytis cinerea. The reduced symptoms of transformed plants have been related to the inability of the pathogens to take advantage of host PMEs and to their impaired ability to grow on methylesterified pectins.