Pectin methylesterase is required for susceptibility to necrotrophic pathogens and for Turnip Vein Clearing Virus spreading in Arabidopsis thaliana.

The majority of fungi and bacteria have evolved the ability to cleave the polysaccharides of the cell wall to release nutrients that sustain their growth and tissue colonization. The production of pectic enzymes, such as pectin methylesterases (PMEs) and polygalacturonases (PGs), is the pre-requisite for subsequent cell wall degradation by other hydrolytic enzymes. Evidence indicates that variation of methylesterification of pectin affects plant defense. PME knockout and over-expression of pectin methylesterase inhibitors (PMEIs) have been used to reduce PME activity in planta. We show here that growth of two necrotrophic pathogens is affected by host PME activity which is induced by the pathogens and play a role as a susceptibility factor. PME is also involved in virus infection. Interaction between the tobacco mosaic virus (TMV) movement protein (MP) and host PME is required for viral cell-to-cell and systemic movement. Our results indicate that PMEIs control the function of PME as host-receptor of viral MP and can be used as a tool for improving resistance of A.thaliana to the Turnip vein clearing virus.