Subtilases turn on pectin methylesterase activity for a robust apoplastic immunity

Plants involve a fine modulation of pectin methylesterase (PME) activity against microbes. PME activity can promote the cell wall stiffening and the production of damage signals able to induce defense responses. However, to date, the knowledge about the molecular mechanisms triggering PME activity during disease remains largely unknown. In this study, we explored the role of subtilases (SBTs), serine proteases consisting of 56 isoforms in Arabidopsis thaliana, as activators of PME activity in plant immunity. By using biochemical and reverse genetic approaches, we found that SBT3.3 and SBT3.5 are required to control PME activity and resistance to the fungus Botrytis cinerea. Arabidopsis sbt3.3 and sbt3.5 knockout mutants showed a reduced induction of PME activity and an increased susceptibility to B. cinerea. SBT3.3 expression is controlled by the damage-associated molecular patterns Oligogalacturonides. The SBT3.3 overexpression overactivates PME activity, but only during fungal infection, resulting in an increased expression of the defense-related genes and in an enhanced resistance to B. cinerea. We revealed that SBT3.3 and the Pro-PME17 isoforms are both secreted in the cell wall exploiting distinct protein secretion pathways and a different kinetic. Our findings point to SBTs as a mechanism to switch on PME activity and the related pectin integrity signaling to strengthen plant immunity against pests, in a timely manner to avoid the growth-defense trade-off. One sentence SummarySubtilases arm pectin methylesterase activity against pathogens to switch on pectin integrity signalling, reinforcing plant immunity and avoiding the growth-defense trade-offs