Different Infection Structures and Point Mutation of Diaporthe citri Showing Resistant against Systemic Fungicides

Summary

Citrus melanose, a serious fungal disease affecting citrus crops, is increasingly difficult to control due to the development of fungicide-resistant fungal strains. This study examined how resistant and susceptible Diaporthe citri strains respond to two common fungicides. The researchers found that resistant strains have genetic mutations that allow them to overcome fungicide treatments, particularly a specific change in the β-tubulin gene. Understanding these resistance mechanisms is crucial for developing better strategies to manage citrus diseases.

Background

Citrus melanose, caused by Diaporthe citri, is a serious disease affecting citrus crops causing over 95% damage without control measures. Frequent fungicide applications to manage this disease have led to the development of fungicide-resistant isolates.

Objective

To compare infection behaviors of fungicide-resistant and susceptible D. citri isolates on citrus leaves treated with benomyl and kresoxim-methyl, and to identify genetic mutations responsible for fungicide resistance.

Results

Resistant isolates showed similar germination and hyphal growth on both treated and untreated leaves, while susceptible isolates were inhibited by fungicide pre-treatment. A point mutation at amino acid 198 of β-tubulin gene (alanine instead of glutamic acid) was found in the benomyl-resistant isolate NEL21-2. No cytochrome b mutations were found in kresoxim-methyl resistant isolates, suggesting alternative resistance mechanisms.

Conclusion

The point mutation at β-tubulin position 198 confers benomyl resistance in D. citri, while kresoxim-methyl resistance appears to result from genetic changes other than cytochrome b mutations. These findings enhance understanding of fungicide resistance mechanisms in D. citri.
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