Plant pathogens negatively affect agricultural production by reducing the plant yield and worsening the nutritional and qualitative characteristics of the harvest. To limit the damage caused by pathogen infection, crops are treated with large doses of pesticides, which cause soil and groundwater pollution. The use of crop varieties genetically resistant to necrotrophs represents a more sustainable solution but is limited by the scarcity of resistance genes to be integrated into crops. For this reason, the identification of new

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. Arabidopsissbt3.3 and sbt3.5 knockout mutants showed a reduced induction of PME activity and an increased susceptibility to B. cinerea. The SBT3.3 overexpression overactivates PME activity only during fungal infection resulting in an increased expression of the defence-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 using a conventional protein secretion pathway and their colocalization in the apoplast increase over time. Our findings point to SBTs as a mechanism to switch on pectin integrity signaling and to reinforce plant immunity at the right time to avoid the growth-defense trade-off.

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