For many years wood decay by fungi was assumed to be caused exclusively by extracellular cellulases and lignin degrading peroxidase enzymes produced by certain Ascomycota and Basidiomycota species. It is now recognized that enzymatic action alone does not explain how "brown rot" wood decay occurs. A non-enzymatic pathway generating hydroxyl radicals deep within wood cell walls has now been demonstrated to be responsible for the depolymerization of both cellulose and lignin during brown rot wood decay, and extracellular cellulases are then produced secondarily to permit further deconstruction of the plant cell walls. Because iron-binding compounds mediate this degradation of wood, the mechanism observed has been termed the "chelator-mediated Fenton" (CMF) reaction. Decay species such as Fomitiporia mediterranea (Fmed) are intermediate between brown and white rot fungi and this species is known to be involved in Esca disease in Vitis vinifera. However, it is unknown whether Fmed or other grapevine trunk disease fungal species produce low molecular weight (LMW) iron-binding compounds to promote CMF reactions and wood decay. The aim of our work is to better understand the role of CMF reactions in lignum during Esca infection in order to develop control strategies. Indeed, assuming that the iron-binding and the redox capacity of the LMW metabolites from the pathogen may be important in disease development, any Biological Control Agent (BCA) that could play a role in interfering with the fungal CMF mechanism may help to reduce the pathogenic effects and spread of the causal fungi. For this purpose, we are investigating the ability of the fungi associated with Esca to produce iron-binding metabolites and oxalic acid; both playing an essential role in the CMF reaction. We are also considering the degradation capacity of oxalic acid by different Trichoderma species to explore if oxalate oxidase increases the activity of these biocontrol agents.
Non-Enzymatic in lignum degradation mechanism: a way to control Grapevine Trunk Disease?
STEFANO DI MARCO;
2019
Abstract
For many years wood decay by fungi was assumed to be caused exclusively by extracellular cellulases and lignin degrading peroxidase enzymes produced by certain Ascomycota and Basidiomycota species. It is now recognized that enzymatic action alone does not explain how "brown rot" wood decay occurs. A non-enzymatic pathway generating hydroxyl radicals deep within wood cell walls has now been demonstrated to be responsible for the depolymerization of both cellulose and lignin during brown rot wood decay, and extracellular cellulases are then produced secondarily to permit further deconstruction of the plant cell walls. Because iron-binding compounds mediate this degradation of wood, the mechanism observed has been termed the "chelator-mediated Fenton" (CMF) reaction. Decay species such as Fomitiporia mediterranea (Fmed) are intermediate between brown and white rot fungi and this species is known to be involved in Esca disease in Vitis vinifera. However, it is unknown whether Fmed or other grapevine trunk disease fungal species produce low molecular weight (LMW) iron-binding compounds to promote CMF reactions and wood decay. The aim of our work is to better understand the role of CMF reactions in lignum during Esca infection in order to develop control strategies. Indeed, assuming that the iron-binding and the redox capacity of the LMW metabolites from the pathogen may be important in disease development, any Biological Control Agent (BCA) that could play a role in interfering with the fungal CMF mechanism may help to reduce the pathogenic effects and spread of the causal fungi. For this purpose, we are investigating the ability of the fungi associated with Esca to produce iron-binding metabolites and oxalic acid; both playing an essential role in the CMF reaction. We are also considering the degradation capacity of oxalic acid by different Trichoderma species to explore if oxalate oxidase increases the activity of these biocontrol agents.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.