ArticleScientific reports2015
The Y137H mutation of VvCYP51 gene confers the reduced sensitivity to tebuconazole in Villosiclava virens.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Article
- The Bacteria-Derived dsRNA Was Used for Spray-Induced Gene Silencing for Rice False Smut Control.Journal of agricultural and food chemistry · 2024Article
- Baseline tebuconazole sensitivity and potential resistant risk in Fusarium Graminearum.BMC plant biology · 2024Article
- SntB Affects Growth to Regulate Infecting Potential inJournal of fungi (Basel, Switzerland) · 2024Article
- Sensitivity Baselines, Resistance Monitoring, and Molecular Mechanisms of the Rice False Smut PathogenJournal of fungi (Basel, Switzerland) · 2023Article
- In Vitro Evaluation of Azoxystrobin, Boscalid, Fentin-Hydroxide, Propiconazole, Pyraclostrobin Fungicides againstMicroorganisms · 2023Article
- Prevalence of Carbendazin Resistance in Field Populations of the Rice False Smut PathogenJournal of fungi (Basel, Switzerland) · 2022Article
- Reproduction response of Colletotrichum fungi under the fungicide stress reveals new aspects of chemical control of fungal diseases.Microbial biotechnology · 2022Article
- Molecular characterization and overexpression of the difenoconazole resistance gene CYP51 in Lasiodiplodia theobromae field isolates.Scientific reports · 2021Article
- Characterization ofApplied and environmental microbiology · 2021Article
- Selection Pressure Pathways and Mechanisms of Resistance to the Demethylation Inhibitor-Difenoconazole inFrontiers in microbiology · 2018Article
- Demethylase Inhibitor Fungicide Resistance in Pyrenophora teres f. sp. teres Associated with Target Site Modification and Inducible Overexpression of Cyp51.Frontiers in microbiology · 2016Article
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7 authors.
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Abstract
Management of rice false smut disease caused by Villosiclava virens is dependent on demethylation inhibitor (DMI) fungicides. Investigation of molecular mechanisms of resistance is therefore of upmost importance. In this study the gene encoding the target protein for DMI fungicides (VvCYP51) was cloned and investigated. The VvCYP51 gene in the resistant mutant revealed both a change from tyrosine to histidine at position 137 (Y137H) and elevated gene expression compared to the parental isolate. In order to determine which of these mechanisms was responsible for the reduced sensitivity to DMI fungicide tebuconazole, transformants expressing the mutated or the wild type VvCYP51 gene were generated. Transformants carrying the mutated gene were more resistant to tebuconazole compared to control transformants lacking the mutation, but the expression of the VvCYP51 gene was not significantly correlated with EC50 values. The wild type VvCYP51 protein exhibited stronger affinity for tebuconazole compared to the VvCYP51/Y137H in both molecular docking analysis and experimental binding assays. The UV-generated mutant as well as transformants expressing the VvCYP51/Y137H did not exhibit significant fitness penalties based on mycelial growth and spore germination, suggesting that isolates resistant to DMI fungicides based on the Y137H mutation may develop and be competitive in the field.
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