Pathogenic Mechanisms of Sclerotinia sclerotiorum in Plant Systems

Sclerotinia sclerotiorum is a broadly necrotrophic ascomycete responsible for white mould disease in over 600 plant species. It survives in soil as sclerotia, initiates infection through oxalic acid secretion which acidifies host tissues and suppresses early defences, then deploys an array of hydrolytic enzymes and small secreted effectors to breach cell walls and induce programmed cell death. A transient biotrophic-like phase facilitates host penetration, followed by a necrotrophic phase marked by reactive oxygen species accumulation and tissue collapse. Genomic and transcriptomic analyses have revealed temporal coordination of carbohydrate-active enzymes, secretome components and redox-modulating factors, shedding light on quantitative disease resistance in crops and informing strategies for durable control.

Research from Nature Portfolio

Recent studies have identified a secreted laccase, Sslac2, as central to environmental sensing and virulence in S. sclerotiorum. Deletion of the corresponding gene abolishes pathogenicity, alters extracellular matrix structure and disrupts perception of host cues, while host-induced silencing of Sslac2 significantly enhances plant resistance. Comparative genomic and transcriptional work has also expanded the catalogue of carbohydrate-active enzymes, showing that genes for both plant cell wall degradation and fungal cell wall remodelling are upregulated during infection. This body of work further highlighted a small cysteine-rich protein essential for virulence and sclerotial development, underlining the pivotal role of secretome components in broad-host-range necrotrophy.

Pathogenic Mechanisms of Sclerotinia sclerotiorum in Plant Systems publication trend

The graph below shows the total number of articles in pathogenic mechanisms of sclerotinia sclerotiorum in plant systems across all publications each year (not limited to Nature Index journals).

Technical terms

Necrotroph: A pathogen that kills host cells and feeds on their remains.

Sclerotium: A hardened, multicellular fungal structure enabling long-term survival in soil.

Oxalic acid: A secreted dicarboxylic acid that acidifies host tissue and modulates redox balance.

Carbohydrate-active enzymes (CAZymes): Enzymes that degrade or modify plant and fungal cell wall polysaccharides.

Secretome: The complete set of proteins secreted by a pathogen during infection.

Host-induced gene silencing (HIGS): A strategy whereby plants produce RNA molecules to silence specific pathogen genes.

References

1. Tipping the Balance: Sclerotinia sclerotiorum Secreted Oxalic Acid Suppresses Host Defenses by Manipulating the Host Redox Environment. PLOS Pathogens (2011).
2. Comparative genomic and transcriptional analyses of the carbohydrate-active enzymes and secretomes of phytopathogenic fungi reveal their significant roles during infection and development. Scientific Reports (2015).
3. Changes in the Sclerotinia sclerotiorum transcriptome during infection of Brassica napus. BMC Genomics (2017).
4. A single laccase acts as a key component of environmental sensing in a broad host range fungal pathogen. Communications Biology (2024).
5. A Small Secreted Virulence-Related Protein Is Essential for the Necrotrophic Interactions of Sclerotinia sclerotiorum with Its Host Plants. PLOS Pathogens (2016).
6. A GDP-mannose-1-phosphate guanylyltransferase as a potential HIGS target against Sclerotinia sclerotiorum. PLOS Pathogens (2025).
7. Recent strategies for controlling the white mould fungal pathogen ( Sclerotinia sclerotiorum ) using gene silencing, botanical fungicides and nanomaterials. Sustainable Food Technology (2025).