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Resistance risk asssement and molecular basis of metconazole in Fusarium pseudograminearum
Guixiang Li1, Yiwen Li1, Ling Zhang1
1State Key Laboratory for Crop Stress Resistance and High-Efficiency Production, College of Plant Protection, Northwest A&F University, 3 Taicheng Road, Yangling, Shaanxi, 712100, China.
Abstract:
The fungicide metconazole, which acts as a sterol 14α-demethylation inhibitor (DMI), can exhibit strong inhibitory effects on Fusarium pseudograminearum. However, the resistance mechanism as well as the risk that F. pseudograminearum develops resistance to metconazole is yet to be fully assessed. In this study, metconazole displayed a mean EC50 value of 0.0559 μg/mL against 105 F. pseudograminearum isolates. Ten sensitive parental isolates were then subjected to fungicide adaptation to generate resistant mutants, with in vitro experiments subsequently highlighting the inferior fitness of the mutants. In addition, metconazole exhibited positive cross-resistance with both mefentrifluconazole and tebuconazole. Altogether, the results confirmed the low risk that F. pseudograminearum develops resistance to metconazole. Finally, a mutation genotype (M151T) was identified in FpCYP51B, with the mutants also overexpressing the FpCYP51 genes. Subsequent molecular docking and transformation-based experiments indicated that M151T substitution and overexpression in FpCYP51 genes conferred resistance to metconazole in F. pseudograminearum.
Insights
Fusarium pseudograminearum shows low risk of developing resistance to the fungicide metconazole. Mutations in FpCYP51B genes, specifically M151T, and gene overexpression confer resistance, though mutants have reduced fitness.
Area of Science:
- Agricultural Science
- Mycology
- Biochemistry
Background:
- Metconazole, a sterol 14α-demethylation inhibitor (DMI) fungicide, effectively inhibits Fusarium pseudograminearum.
- Understanding the resistance mechanisms and risk of F. pseudograminearum developing resistance to metconazole is crucial for effective disease management.
Purpose of the Study:
- To assess the resistance risk of F. pseudograminearum to metconazole.
- To identify the genetic and molecular mechanisms underlying metconazole resistance in F. pseudograminearum.
Main Methods:
- Determined the EC50 of metconazole against F. pseudograminearum isolates.
- Generated resistant mutants through fungicide adaptation and assessed their fitness.
- Investigated cross-resistance with other DMI fungicides.
- Identified mutations and gene expression changes in resistant mutants using molecular techniques.
Main Results:
- Metconazole exhibited a low EC50 value (0.0559 μg/mL) against F. pseudograminearum.
- Resistant mutants displayed reduced in vitro fitness.
- Positive cross-resistance was observed with mefentrifluconazole and tebuconazole.
- The M151T mutation in FpCYP51B and overexpression of FpCYP51 genes were identified as key resistance mechanisms.
Conclusions:
- F. pseudograminearum has a low risk of developing resistance to metconazole due to reduced mutant fitness.
- The M151T substitution in FpCYP51B and FpCYP51 gene overexpression confer metconazole resistance.
- These findings provide insights into fungicide resistance management strategies for Fusarium diseases.
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Fungal Group Zygomycota
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