Fungicide Resistance Mechanisms in Plant Pathogenic Fungi

Fungicide resistance in plant pathogenic fungi arises through a spectrum of molecular and cellular adaptations that undermine disease control efforts worldwide. The most widely documented mechanism is target-site modification, where point mutations in key enzymes such as sterol demethylases or succinate dehydrogenases reduce fungicide binding without abolishing enzyme function. Equally important are non-target-site mechanisms, including overexpression of efflux transporters that actively expel fungicidal molecules, and promoter rearrangements that drive elevated transcription of target genes. Recent discoveries have also highlighted the role of standing genetic variation and paralogous gene re-emergence in conferring resistance to novel chemistries, illustrating how pre-existing alleles within a population can be rapidly selected under fungicide pressure. These mechanisms often act in combination, leading to multidrug resistance phenotypes that persist in the field without apparent fitness penalties. The global spread of resistant strains threatens the efficacy of single-site fungicides and calls for integrated stewardship strategies, such as dose optimisation, mixture of modes of action and continual monitoring to preserve the durability of chemical controls in agriculture.

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Fungicide Resistance Mechanisms in Plant Pathogenic Fungi publication trend

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

Technical terms

Target-site mutation: An amino acid change in a fungicide’s molecular target that lowers binding affinity while preserving enzymatic activity.

Efflux transporter: A membrane protein that exports toxic compounds, including fungicides, from the fungal cell to confer resistance.

Standing genetic variation: Pre-existing genetic diversity within a population that can be rapidly selected under chemical pressure.

Paralog: A gene duplicate arising from genome duplication or rearrangement that may acquire novel functions or confer resistance.

Mode of action: The specific biochemical interaction through which a fungicide inhibits a fungal target, such as demethylation inhibition or ubiquinone binding.

References

1. The Emergence of Resistance to Fungicides. PLOS ONE (2014).
2. Paralog Re-Emergence: A Novel, Historically Contingent Mechanism in the Evolution of Antimicrobial Resistance. Molecular Biology and Evolution (2014).
3. Fungicide Resistance in Powdery Mildew Fungi. Microorganisms (2020).
4. Fungicide Resistance Evolution and Detection in Plant Pathogens: Plasmopara viticola as a Case Study. Microorganisms (2021).
5. A dispensable paralog of succinate dehydrogenase subunit C mediates standing resistance towards a subclass of SDHI fungicides in Zymoseptoria tritici. PLOS Pathogens (2019).