Pectins, major components of dicot cell walls, are synthesized in a heavily methylesterified form in the Golgi and are partially deesterified by pectin methylesterases (PMEs) upon export to the cell wall. PME activity is important for the virulence of the necrotrophic fungal pathogen Botrytis cinerea. Here, the roles of Arabidopsis PMEs in pattern-triggered immunity and immune responses to the necrotrophic fungus Alternaria brassicicola and the bacterial hemibiotroph Pseudomonas syringae pv maculicola ES4326 (Pma ES4326) were studied. Plant PME activity increased during pattern-triggered immunity and after inoculation with either pathogen. The increase of PME activity in response to pathogen treatment was concomitant with a decrease in pectin methylesterification. The pathogen-induced PME activity did not require salicylic acid or ethylene signaling, but was dependent on jasmonic acid signaling. In the case of induction by A. brassicicola, the ethylene response factor, but not the MYC2 branch of jasmonic acid signaling, contributed to induction of PME activity, whereas in the case of induction by Pma ES4326, both branches contributed. There are 66 PME genes in Arabidopsis, suggesting extensive genetic redundancy. Nevertheless, selected pme single, double, triple and quadruple mutants allowed significantly more growth of Pma ES4326 than wild-type plants, indicating a role of PMEs in resistance to this pathogen. No decreases in total PME activity were detected in these pme mutants, suggesting that the determinant of immunity is not total PME activity; rather, it is some specific effect of PMEs such as changes in the pattern of pectin methylesterification.

Loss of UDP-glucuronate 4-epimerases GAE1 and GAE6 in Arabidopsis thaliana causes a dramatic reduction of pectin in the cell wall and compromised immunity to Ps

In Arabidopsis thaliana, mitogen activated protein kinase (MAPK) signaling cascades that contain MPK3, MPK4 and MPK6 have been implicated in various aspects of developmental processes and stress responses. We identified an ethylene response factor (ERF104), which controls innate immunity, to be a specific substrate of MPK6 and showed that ethylene signaling regulates the release of the ERF104 substrate from its kinase. Implications and questions that arise from our findings are addressed. To promote discussions, previously unpublished data, that are rather confounding, are presented and possible explanation provided on how these may fit into our current model.

The goal of this procedure is to extract pectin from plant cell walls. Pectins are galacturonic acid containing polymeric sugars that are important components of plant cell walls. Various procedures aimed at studying plant cell wall components require the extraction of pectin. Pectin is synthesized in the Golgi apparatus in a highly esterified fashion and is de-esterified in the cell wall (Mohnen, 2008). Pectin is generally water soluble. De-esterified pectin can form so-called “egg-box structures” in the presence of Ca2+ ions (Mohnen, 2008; Harholt et al., 2010). Pectin in these “egg-box structures” is cross-linked and less soluble. Cyclohexane diamine tetraacetic acid (CDTA) chelates Ca2+ ions and hence allows extraction of Ca2+ cross-linked pectin from cell walls.