Molecular Mechanisms of Fungal Pathogenicity in Postharvest Diseases

Postharvest decay of fruits and vegetables is predominantly driven by necrotrophic fungi that exploit host tissues through a coordinated arsenal of biochemical and molecular strategies. Initial spore germination at wound sites is followed by adhesion and penetration, often mediated by cell wall–degrading enzymes such as polygalacturonases and pectin lyases. Secretion of organic acids lowers the local pH, optimising enzyme activity and facilitating mycotoxin synthesis. Reactive oxygen species secreted by both pathogen and host trigger oxidative stress responses; fungi deploy antioxidant enzymes to counter host defences. Transcriptional reprogramming is orchestrated by specific transcription factors and chromatin remodelling that activate genes encoding effectors, transporters and secondary metabolism pathways. Epigenetic readers further fine-tune expression of virulence determinants and toxins such as patulin and citrinin. On the host side, pattern-triggered immunity and effector-triggered immunity recruit signalling cascades involving jasmonate and ethylene, while fruit resistance loci modulate defence gene networks. Integration of these insights underpins development of innovative control measures, from targeted fungicide design to biocontrol deployment and storage-condition optimisation, with potential to reduce global food losses and mycotoxin risks.

Research from Nature Portfolio

Recent studies have applied high-throughput transcriptome profiling to unravel tri-trophic interactions among a biocontrol yeast, a fungal pathogen and the host fruit. Analysis of a yeast biocontrol agent interacting with the pathogen in apple tissue revealed upregulation of over 800 genes involved in nutrient uptake and oxidative stress defence, suggesting mechanisms by which the yeast outcompetes the pathogen. Concurrent profiling of the pathogen highlighted more than 1,000 genes activated in transcription regulation, redox metabolism and membrane transport. The host fruit exhibited a pronounced defence signature, with induction of both pattern-triggered and effector-triggered immunity pathways when challenged by the pathogen, illuminating key molecular dialogues that underpin successful biocontrol and host protection.

Molecular Mechanisms of Fungal Pathogenicity in Postharvest Diseases publication trend

The graph below shows the total number of articles in molecular mechanisms of fungal pathogenicity in postharvest diseases across all publications each year (not limited to Nature Index journals).

Technical terms

Necrotroph: a fungus that kills host cells and derives nutrients from dead tissues.

Effector: a secreted molecule that manipulates host processes to facilitate infection.

Pattern-triggered immunity (PTI): the plant’s initial defence response activated by recognition of conserved pathogen molecules.

Effector-triggered immunity (ETI): a robust host response initiated by detection of specific pathogen effectors.

ATAC-seq: a technique to map accessible regions of chromatin, indicating active regulatory elements.

Differentially expressed genes (DEGs): genes showing significant changes in expression under different conditions.

Epigenetic reader: a protein that recognises specific chromatin marks to regulate gene expression.

References

1. Chromatin accessibility profile and the role of PeAtf1 transcription factor in the postharvest pathogen Penicillium expansum. Horticulture Research (2024).
2. Transcriptomic investigation of the interaction between a biocontrol yeast, Papiliotrema terrestris strain PT22AV, and the postharvest fungal pathogen Penicillium expansum on apple. Communications Biology (2024).
3. Penicillium expansum: biology, omics, and management tools for a global postharvest pathogen causing blue mould of pome fruit. Molecular Plant Pathology (2020).
4. Study on the Infection Mechanism of Penicillium Digitatum on Postharvest Citrus (Citrus Reticulata Blanco) Based on Transcriptomics. Microorganisms (2019).
5. New Insight Into Pathogenicity and Secondary Metabolism of the Plant Pathogen Penicillium expansum Through Deletion of the Epigenetic Reader SntB. Frontiers in Microbiology (2020).