Resistance risk and molecular mechanism associated with resistance to picoxystrobin in Colletotrichum truncatum and Colletotrichum gloeosporioides

Shi, Niuniu; Lian, Jia; Qiu, Dunlian; Chen, Furu; Du, Yongle

doi:10.1016/j.jia.2023.07.037

Journal of Integrative Agriculture

2023

DOI: 10.1016/j.jia.2023.07.037

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Resistance risk and molecular mechanism associated with resistance to picoxystrobin in Colletotrichum truncatum and Colletotrichum gloeosporioides

Niuniu Shi

Jia Lian

Dunlian Qiu

et al.

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2024

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Cited by 3 publications

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Resistance risk assessment of Rhizoctonia solani to four fungicides

Ou,

Hu,

et al. 2024

Pest Management Science

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BACKGROUNDHexaconazole, thifluzamide, difenoconazole and azoxystrobin are widely used fungicides for the control of Rhizoctonia solani in China. However, few studies have assessed the sensitivity and resistance risk of R. solani to these four fungicides.RESULTSThe sensitivities of 126 R. solani isolates to hexaconazole, thifluzamide, difenoconazole and azoxystrobin were determined, with average half maximal effective concentration (EC50) values of 0.0386, 0.0659, 0.663 and 1.508 μg mL−1, respectively. Field resistance monitoring of the four fungicides showed that the three isolates had moderate resistance to difenoconazole. Resistant mutants to the four fungicides were obtained by fungicide adaptation, and resistance could be stably inherited by most mutants. Compared with those of the parent isolates, the biological characteristics of hexaconazole‐resistant mutants exhibited enhanced or similar compound fitness index (CFI), whereas most of the other mutants displayed reduced or comparable CFI. There was evidence of positive cross‐resistance between hexaconazole and difenoconazole. In the presence of fungicides, the expression of the CYP51 genes in hexaconazole‐ and difenoconazole‐resistant mutants significantly increased, the expression of SDH genes in thifluzamide‐resistant mutants significantly decreased, and the expression of the Cyt b gene in azoxystrobin‐resistant mutants did not significantly change.CONCLUSIONBased on these data, we speculated that R. solani had a low‐to‐medium resistance risk to four fungicides. The change of target gene expression may be one of the reasons for fungicide resistance in R. solani. This study provides a theoretical basis for monitoring resistance emergence and developing resistance management strategies to control R. solani. © 2024 Society of Chemical Industry.

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Resistance risk assessment of Rhizoctonia solani to four fungicides

Ou,

Hu,

et al. 2024

Pest Management Science

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Revisiting the intron hypothesis of QoI resistance in Phyllosticta ampelicida, the causal agent of grape black rot, and other Phyllosticta species

Horváth,

Molnár,

Németh

et al. 2024

Plant Pathology

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Chemical control of grape black rot, caused by Phyllosticta ampelicida, relies mainly on the use of demethylation inhibitors (DMIs) and quinone outside inhibitors (QoIs). The effectiveness of QoI fungicides is influenced by alternative respiration activity, and the exon/intron structure and point mutations in the target protein's gene, the cytochrome b (cytb) gene. Our study aims to investigate the QoI fungicide sensitivity of 48 P. ampelicida isolates in vitro by measuring EC50 and the molecular characteristics of the cytb gene and its mRNA in P. ampelicida and other Phyllosticta species. Mycelial growth tests revealed that the P. ampelicida isolates were sensitive to both azoxystrobin and trifloxystrobin; baseline EC50 values were 0.029 and 0.022 μg/mL, respectively. Addition of salicylhydroxamic acid (SHAM) resulted in lower EC50 values (0.024 and 0.017 μg/mL, respectively). None of the typical point mutations conferring resistance to QoIs in some fungi were detected. A group I intron was present right after the 143rd codon in the cytb gene in four of the six Phyllosticta species examined. The sequence and exon/intron structure of the cytb gene of P. ampelicida isolated from Vitis vinifera is studied in detail and published here. Our results indicate a low risk of QoI resistance development via the G143A mutation in P. ampelicida.

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Inhibition of Neural Crest Cell Migration by Strobilurin Fungicides and Other Mitochondrial Toxicants

Magel,

Blum,

Dolde

et al. 2024

Cells

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Cell-based test methods with a phenotypic readout are frequently used for toxicity screening. However, guidance on how to validate the hits and how to integrate this information with other data for purposes of risk assessment is missing. We present here such a procedure and exemplify it with a case study on neural crest cell (NCC)-based developmental toxicity of picoxystrobin. A library of potential environmental toxicants was screened in the UKN2 assay, which simultaneously measures migration and cytotoxicity in NCC. Several strobilurin fungicides, known as inhibitors of the mitochondrial respiratory chain complex III, emerged as specific hits. From these, picoxystrobin was chosen to exemplify a roadmap leading from cell-based testing towards toxicological predictions. Following a stringent confirmatory testing, an adverse outcome pathway was developed to provide a testable toxicity hypothesis. Mechanistic studies showed that the oxygen consumption rate was inhibited at sub-µM picoxystrobin concentrations after a 24 h pre-exposure. Migration was inhibited in the 100 nM range, under assay conditions forcing cells to rely on mitochondria. Biokinetic modeling was used to predict intracellular concentrations. Assuming an oral intake of picoxystrobin, consistent with the acceptable daily intake level, physiologically based kinetic modeling suggested that brain concentrations of 0.1–1 µM may be reached. Using this broad array of hazard and toxicokinetics data, we calculated a margin of exposure ≥ 80 between the lowest in vitro point of departure and the highest predicted tissue concentration. Thus, our study exemplifies a hit follow-up strategy and contributes to paving the way to next-generation risk assessment.

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Resistance risk and molecular mechanism associated with resistance to picoxystrobin in Colletotrichum truncatum and Colletotrichum gloeosporioides

Cited by 3 publications

References 45 publications

Resistance risk assessment of Rhizoctonia solani to four fungicides

Resistance risk assessment of Rhizoctonia solani to four fungicides

Revisiting the intron hypothesis of QoI resistance in Phyllosticta ampelicida, the causal agent of grape black rot, and other Phyllosticta species

Inhibition of Neural Crest Cell Migration by Strobilurin Fungicides and Other Mitochondrial Toxicants

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