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Article 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 EC 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12043553 | PMC |
| http://dx.doi.org/10.1007/s44154-025-00221-0 | DOI Listing |
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- Innovative strategies are needed to combat fungal pathogens for sustainable crop protection, with traditional fungicides facing resistance issues due to their single-target action.
- The study investigated the synergistic effects of chitosan (CS) and the fungicide azoxystrobin, finding a high synergy score that significantly improves antifungal efficacy.
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