Molecular factors underlying Arabidopsis PME activation against Botrytis

Cell wall (CW) is the foremost interface at which plants and fungi interactions take place. Pectin is methylesterified in the Golgi and secreted in the CW in a high methylesterified form. The activity of Pectin Methyl Esterase (PMEs) and methylesterification status of pectin are critical for the outcome of plant-fungus interaction. PME activity was associated to the production of de-methyl esterified and active Oligogalacturonides, the best characterized damage-associated molecular patterns (DAMPs) in plants. Moreover, PME is responsible for the release of methanol, which may function as DAMP alerting adjacent non infected tissues or neighbouring plants. The de-methyl esterified pectin can form crosslinks with calcium promoting wall stiffening. However, evidence indicates that pectin de-methylesterification also trigger the degradation by pectinases from pathogens. Despite this evidence, the current knowledge about the molecular mechanisms regulating pectin methylesterase activity during disease remains largely unknown. PME activity can be regulated by subtilisin-like proteases (SBTs) and by PME inhibitors (PMEIs). By using biochemical and reverse genetic approaches we demonstrate the role of specific PMEs and SBTs in plant immunity. PME17 and SBT3.3 emerged as functional pectin methyl esterases regulating PME activity and Arabidopsis resistance against Botrytis attack. The potential mechanisms of regulation and signal transduction triggered by pectin methyl esterase activity during fungal infection will be discussed.