From Antifungal Hydrolases to Modern Plant Immunity: Revisiting the Legacy of Boller

The 1988 papers by Mauch, Mauch-Mani, Hadwiger and Boller on pea antifungal hydrolases captured a simple but powerful idea: plants can attack pathogens by directly targeting the structural polymers that hold their cell walls together. At that time, chitinases and β-1,3-glucanases were known to accumulate after infection, wounding and ethylene treatment, but whether these proteins actually restricted fungal growth remained unclear. By resolving distinct hydrolase isoforms and showing that inducible chitinase and β-1,3-glucanase act synergistically to inhibit fungal growth and lyse hyphal tips, these studies transformed infection-induced enzyme accumulation into a mechanistic model of antifungal activity. We now recognize that fungal cell wall hydrolysis also releases glycan fragments that act as immune signals and are perceived by plant immune receptors, linking pathogen damage to immune activation in plants. At the same time, pathogens have evolved counterstrategies to mask, modify or protect these cell wall components, limiting both enzymatic access and immune detection. Thus, the Boller studies anticipated a central theme of modern molecular plant pathology: plant-pathogen interactions are dynamic interfaces where host enzymes, pathogen wall fragments, immune receptors and pathogen counterstrategies converge.