Subtilases trigger pectin-related immunity against pathogens

Plants involve a spatiotemporal modulation of Immunity triggered-Pectin Methylesterase (IT-PME) activity against microbes 1. IT-PMEs can induce the formation of the “egg-box” structures, resulting in wall stiffening. IT-PME activity can also favour the production of Damage Associated Molecular Patterns (DAMPs). For instance, PMEs can promote the release or perception de-methylesterified Oligogalacturonides (OGs) able to trigger plant immunity. De-methylesterification of pectin by PMEs can also generate the alarm signal Methanol (MeOH). MeOH and OGs are able to trigger a defensive priming in plants 2,3. Moreover, the Pathogen Recognition Receptors (PRRs) Wall Associated Kinase 1 (WAK1), WAK2 and FERONIA (FER) preferentially bind to de-methylesterified pectins 4–6 and RLP44 receptor is required for the response to changes in pectin de-methylesterification7. Despite this evidence, the current knowledge about the molecular mechanisms triggering PME activity during disease remains largely unknown. PME activity can be regulated by subtilases (SBTs), serine proteases consisting of 56 isoforms in Arabidopsis thaliana. SBTs were involved in response to biotic stresses and plant immunity although their physiological substrates remain unknown 8. By using biochemical and reverse genetic approaches, we have identified SBT3.3 and SBT3.5, as functional subtilases specifically induced in Arabidopsis during Botrytis cinerea infection. Both SBTs control IT-PME activity against B. cinerea and contribute to resistance against the fungus. A role of SBT3.3 expression in the release of pectic mucilage also emerged. We are currently focusing on the immune signalling activated by SBTs. Our findings point to SBTs as mediators of pectin integrity maintenance in plant-microbe interactions. The potential mechanisms of modification, perception, and signal transduction of pectin methylesterification in plant defence will be also discussed.