Ricerc@Sapienza

Cell wall (CW) is the foremost interface at which interactions between plants and fungi take place. Pectin, one of the main components of CW, is secreted in a high methylesterified form. Pectin methylesterases (PMEs), catalyse the removal of the methyl esters producing homogalacturonans, releasing methanol (MeOH) and protons. Specific plant PMEs are induced in different plants by necrotrophs but the knowledge of the molecular mechanisms underlying PME-related immunity remain currently limited. PMEs could assist the production of Oligogalacturonides (OGs), elicitors of defence responses. Intriguingly, MeOH, a volatile organic compound released by PME activity, may function as a systemic intra-plant or inter-plant alarm signal. PMEs activity can also reinforce pectin structure, through Ca2+ mediate crosslinks, influencing the penetration of the fungus. PMEs induction could also lead to an apoplast acidification, a potential plant defence response to contrast the host alkalinisation, exploited by Fungi to improve their infectious potential. Available microarray data regarding the expression of Arabidopsis PMEs upon infection by different microbes indicates that AtPME17 is induced by all pathogens analysed and can be considered a potential biomarker for microbial infection. In this project, the contribution of AtPME17 on the PME activity, the release of OGs, MeOH, and changes in apoplastic pH and Ca2+ concentration will be investigated in Arabidopsis during Botrytis cinerea infection. A multidisciplinary approach including reverse genetics, molecular biology, glycan immune-histochemistry, LC-MS/GC-Mass Spectrometry and confocal and electron microscopy will be exploited. The AtPME17 structure and activity and its regulation will be explored by using different biochemical approaches. The project aims to understand if and how AtPME17, and its orthologs in crop species, could represent new promising genetic determinants useful to improve plant resistance to fungal disease.