Exploration of a non-enzymatic wood degradation pathway in Fomitiporia mediterranea, the main white rot pathogen in European Esca-affected vineyards

Fomitiporia mediterranea (Fmed) is identified as a white rot pathogen that has been associated with Esca in European vineyards. This fungus has biomolecular wood degradation mechanisms that are not yet fully understood. White rot has an enzymatic pool (laccases, Class II-peroxidases, carbohydrate-active enzymes) that can degrade lignocellulosic biomass (cellulose, hemicellulose and lignin), leaving grapevine wood as fibrous bleached residues. Comparative genomics and previously reported observations of wood cell microvoid size allowed us to formulate the hypothesis that Fmed could adopt non-enzymatic and enzymatic mechanisms to degrade grapevine wood. This hypothesis is based on the Chelator Mediated Fenton (CMF) model, proposed in the late 1990s by American researchers for brown rot fungi. According to our results, under appropriate experimental conditions as close as possible to the physiological conditions of grapevine wood, Fmed demonstrated in vitro ability to: i) produce low molecular weight (LMW) iron-chelating compounds, which can ii) reduce ferric iron to ferrous iron, and iii) initiate the redox cycle to produce hydroxyl radicals, thus satisfying all the conditions for a CMF-like non-enzymatic wood degradation mechanism. Carbohydrate oxidative experiments also showed that reducing sugars are liberated when cellulose and hemicellulose are treated with the CMF reaction induced by Fmed LMW extracts. Variations in the CMF reaction were observed among different Fmed strains. Research is ongoing to study effectiveness of the nonenzymatic pathway in lignum and in planta.