Botrytis Cinerea Pathogenic Mechanisms and Management Strategies

Botrytis cinerea is a globally pervasive necrotrophic fungal pathogen responsible for grey mould disease across a vast range of economically important crops. Its success hinges on a suite of pathogenic mechanisms including the secretion of hydrolytic enzymes that degrade plant cell walls, the deployment of effector proteins that subvert host immunity, and the formation of specialised penetration structures such as infection cushions. Redundant phytotoxic compounds and cell death-inducing proteins (CDIPs) accelerate host tissue necrosis, liberating nutrients to fuel fungal growth. Management strategies combine cultural practices—crop rotation, canopy ventilation and pruning—with chemical control using fungicides that target respiration or cell wall synthesis. Growing resistance to single-site fungicides has prompted the integration of biological control agents, plant defence elicitors and precision application technologies. Advances in molecular genetics, including marker-free genome editing, have illuminated virulence determinants and offered novel targets for intervention. A holistic approach that unites an understanding of infection biology with sustainable field practices is essential to mitigate losses and preserve crop quality under changing climatic conditions.

Research from Nature Portfolio

Recent studies have revealed that a Major Facilitator Superfamily (MFS) transporter acts as a virulence factor by exporting toxic glucosinolate-breakdown products from the fungal cell, thereby enhancing tolerance to host-derived compounds and promoting infection on cruciferous plants. Functional analyses demonstrated that mutants lacking this transporter accumulate higher levels of isothiocyanates, exhibit reduced virulence and confirm that efflux mechanisms are central to pathogen survival in glucosinolate-rich tissues.

Botrytis Cinerea Pathogenic Mechanisms and Management Strategies publication trend

The graph below shows the total number of articles in botrytis cinerea pathogenic mechanisms and management strategies across all publications each year (not limited to Nature Index journals).

Technical terms

Necrotrophic pathogen: A microorganism that kills host cells to extract nutrients.

Effector protein: A secreted molecule that interferes with host defence or cellular processes.

Infection cushion: A multicellular hyphal structure specialised for penetrating plant tissues.

Major Facilitator Superfamily (MFS) transporter: A membrane protein that exports or imports small molecules across the cell membrane.

Cell Death-Inducing Proteins (CDIPs): Secreted fungal proteins that trigger programmed cell death in host plants.

References

1. Plant triterpenoid saponins function as susceptibility factors to promote the pathogenicity of Botrytis cinerea. Molecular Plant (2024).
2. Characterization of two SGNH family cell death-inducing proteins from the horticulturally important fungal pathogen Botrytis cinerea based on the optimized prokaryotic expression system. Molecular Horticulture (2024).
3. MFS transporter from Botrytis cinerea provides tolerance to glucosinolate-breakdown products and is required for pathogenicity. Nature Communications (2019).
4. CRISPR/Cas with ribonucleoprotein complexes and transiently selected telomere vectors allows highly efficient marker-free and multiple genome editing in Botrytis cinerea. PLOS Pathogens (2020).
5. Multiple knockout mutants reveal a high redundancy of phytotoxic compounds contributing to necrotrophic pathogenesis of Botrytis cinerea. PLOS Pathogens (2022).