Pectin and pathogen susceptibility: loss of non-host resistance to Pseudomonas syringae in Arabidopsis pectinmethylesterase inhibitor mutants
Asier Largo-Gosens (Spain)1 2; Daniel Fernández-García (Spain)1; José Luis Martín (Spain)1 2; María Fuertes-Rabanal (Spain)1 2; Carlota Cerezo (Spain)1 2; Penélope García-Angulo (Spain)1 2;
1 - Área de Fisiología Vegetal, Departamento de Ingeniería y Ciencias Agrarias, Universidad de León, León, España; 2 - Instituto de Biología Molecular, Genómica y Proteómica (INBIOMIC), Universidad de León, León, España.;
Keywords: Homogalacturonan methylation; Pectinmethyesterase inhibitors; Pathogen resistance;
Abstract Topics: Theme 9: Cell Wall Function and Signaling in plant adaptation to Biotic and Abiotic Stresses
Type of Presentation: Poster

Abstract text: Pectin plays a key role in plant development and responses to biotic stresses. The degree and pattern of homogalacturonan (HG) methylesterification are regulated in muro by pectin methylesterases (PMEs) and their specific inhibitors (PMEIs). This determines the fate of HG: it can either form calcium-mediated crosslinks that strengthen the cell wall or be degraded by pectinases, releasing oligogalacturonides with immunomodulatory activity. Therefore, HG demethylation is considered an important component of plant defense responses to pathogen infection.
We previously observed that mutants lacking specific PMEI proteins (pmei3 and pmei13) lose non-host resistance to Pseudomonas syringae pv. phaseolicola (Pph), suggesting that PMEIs play an important role during infection. To better understand this process, we analyzed changes in cell wall composition and cellular responses in these mutants during Pph infection.
Both mutants showed increased susceptibility to Pph but with contrasting responses. In pmei13, PME activity was elevated and cell wall composition strongly altered even without the pathogen that caused limited additional changes. In contrast, pmei3 showed increased PME activity but a cell wall similar to Col-0 plants. However, infection triggered further increases in PME activity and extensive cell wall reorganization. These results suggest that the two mutants affect different resistance strategies to Pph.