Model of PMEI involvement in plant immunity against fungal pathogens. The plant cell wall is the first barrier against pathogen attack. Above all, PME is required for the release of MeOH, H⁺, and pectin-COO⁻ during pathogen infection. MeOH, a DAMP-like alarm signal, down-regulates the expression of the pathogen-related GhPMEI3. H⁺ ions affect the pH of the plant cell wall and promote the hydrolysis of VdPG1 to homogalacturonan. Pectin-COO⁻, with exposed negatively charged groups, binds cations. Al³⁺ ions affect the methylation status of pectin in root cell walls and regulate PME activity. Pectin methyl esterification affects the release and the type of OGs. Moreover, PGIP interacts with PG, which leads to the accumulation of OGs. OGs elicit an antipathogen defense and promote signal transduction in plant cells. Lastly, PMEI is unable to directly inhibit the activity of fungal PMEs and fungal PGs. However, it is possible that GhPMEI3 interacts with plant GhPME2 and GhPME31, reducing the capacity of VdPG1 to hydrolyze methyl esterified pectin and protecting the plant cell wall from degradation.