Three pectin methylesterase inhibitors protect cell wall integrity for arabidopsis immunity to Botrytis

Infection by necrotrophs is a complex process that starts with the breakdown of the cell wall (CW) matrix initiated by CW degrading enzymes and results in an extensive tissue maceration. Plants exploit induced defense mechanisms based on biochemical modification of the CW components to protect themselves from enzymatic degradation. The pectin matrix is the main CW target of Botrytis cinerea and pectin methylesterification status is strongly altered in response to infection. The methylesterification of pectin is mainly controlled by pectin methylesterases (PMEs) which activity is post-transcriptionally regulated by endogenous protein inhbibitors (PMEIs). Here, AtPMEI10, AtPMEI11 and AtPMEI12 are identified as functional pectin methylesterase inhibitors induced in Arabidopsis during Botrytis infection. AtPMEIs expression is strictly regulated by Jasmonic Acid and Ethylene signaling while only AtPMEI11 expression is controlled by PME-related DAMPs, such as oligogalacturonides and methanol. The decrease of pectin methylesterification during infection is higher and the immunity to Botrytis compromised in pmei10, pmei11 and pmei12 mutants respect to the control plants. A higher stimulation of the fungal oxalic acid bioshynthetic pathway can also contribute to the higher susceptibility of pmei mutants. The lack of PMEIs expression do not affect hemicellulose strengthening, callose deposition and synthesis of structural defence proteins, proposed as CW remodeling mechanisms exploited by Arabidopsis to resist to the CW degradation upon Botrytis infection. We showed that PME activity and pectin methylesterification are dynamically modulated by PMEIs during Botrytis infection. Our findings point to AtPMEI10, AtPMEI11 and AtPMEI12 as mediators of CW integrity maintenance in plant immunity.