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Fusarium pseudograminearum, the causal agent of Fusarium crown rot, poses a significant threat to cereal crops. Building upon our previous investigation of the transcriptional response of this pathogen to four key fungicides (carbendazim, phenamacril, pyraclostrobin, and tebuconazole), this study delves into the impact of elevated fungicide concentrations using RNA-seq. Global transcriptomic analysis and gene clustering revealed significant enrichment of genes involved in the ABC transporter pathway. Among these transporters, FPSE_06011 (FpZRA1), a conserved gene in eukaryotes, exhibited consistent upregulation at both low and high fungicide concentrations. Targeted deletion of FpZRA1 resulted in reduced sporulation, spore germination, and tolerance to cell wall stress, osmotic stress, and oxidative stress. Furthermore, the FpZRA1 knockout mutants exhibited decreased pathogenicity on wheat coleoptiles and reduced production of the mycotoxin deoxynivalenol (DON), as evidenced by the markedly down-regulated expression of TRI5, TRI6, and TRI10 in the RT-qPCR analysis. In summary, our findings highlight the impact of fungicide concentration on transcriptional reprogramming in F. pseudograminearum and identify FpZRA1 as a critical regulator of fungal development, stress tolerance, and pathogenicity., Competing Interests: Declaration of competing interest The authors declare no conflict of interest, (Copyright © 2024 Elsevier B.V. All rights reserved.)

Fusarium graminearum is an economically important phytopathogenic fungus. Chemical control remains the dominant approach to managing this plant pathogen. In the present study, we performed a comparative transcriptome analysis to understand the effects of four commercially used fungicides on F. graminearum. The results revealed a significant number of differentially expressed genes related to carbohydrate, amino acid, and lipid metabolism, particularly in the carbendazim and phenamacril groups. Central carbon pathways, including the TCA and glyoxylate cycles, were found to play crucial roles across all treatments except tebuconazole. Weighted gene co-expression network analysis reinforced the pivotal role of central carbon pathways based on identified hub genes. Additionally, critical candidates associated with ATP-binding cassette transporters, heat shock proteins, and chitin synthases were identified. The crucial functions of the isocitrate lyase in F. graminearum were also validated. Overall, the study provided comprehensive insights into the mechanisms of how F. graminearum responds to fungicide stress., Competing Interests: Declaration of competing interest The authors declare that they have no competing interests., (Copyright © 2024. Published by Elsevier Inc.)

Soybean root rot is a worldwide soil-borne disease threatening soybean production, causing large losses in soybean yield and quality. Fusarium species are the most detrimental pathogens of soybean root rot worldwide, causing large production losses. Fusarium root rot has been frequently reported in Heilongjiang Province of China, but the predominant Fusarium species and the sensitivity of these pathogens to different fungicides remain unclear. In this study, diseased soybean roots were collected from 14 regions of Heilongjiang province in 2021 and 2022. A total of 144 isolates of Fusarium spp. were isolated and identified as seven distinct species: F. scirpi, F. oxysporum, F. graminearum, F. clavum, F. acuminatum, F. avenaceum, and F. sporotrichioide. F. scirpi and F. oxysporum had high separation frequency and strong pathogenicity. The sensitivity of Fusarium spp. to five different fungicides was determined. Mefentrifluconazole and fludioxonil showed good inhibitory effects, and the sensitivity to pydiflumetofen and phenamacril varied between Fusarium species. In particular, the activity of DMI fungicide prothioconazole was lower than that of mefentrifluconazole. Molecular docking showed that mefentrifluconazole mainly bound to CYP51C, but prothioconazole mainly bound to CYP51B. Furthermore, the sensitivity to prothioconazole only significantly decreased in ΔFgCYP51B mutant, and the sensitivity to mefentrifluconazole changed in ΔFgCYP51C and ΔFgCYP51A mutants. The results demonstrated that the predominant Fusarium species causing soybean root rot in Heilongjiang province were F. scirpi and F. oxysporum and DMI fungicides had differences in binding cavity due to the diversity of CYP51 proteins in Fusarium., (Copyright © 2023. Published by Elsevier Inc.)

Fusarium head blight in wheat is caused by Fusarium graminearum, resulting in significant yield losses and grain contamination with deoxynivalenol (DON), which poses a potential threat to animal health. Cyclobutrifluram, a newly developed succinate dehydrogenase inhibitor, has shown excellent inhibition of Fusarium spp. However, the resistance risk of F. graminearum to cyclobutrifluram and the molecular mechanism of resistance have not been determined. In this study, we established the average EC 50 of a range of F. graminearum isolates to cyclobutrifluram to be 0.0110 μg/mL. Six cyclobutrifluram-resistant mutants were obtained using fungicide adaptation. All mutants exhibited impaired fitness relative to their parental isolates. This was evident from measurements of mycelial growth, conidiation, conidial germination, virulence, and DON production. Interestingly, cyclobutrifluram did not seem to affect the DON production of either the sensitive isolates or the resistant mutants. Furthermore, a positive cross-resistance was observed between cyclobutrifluram and pydiflumetofen. These findings suggest that F. graminearum carries a moderate to high risk of developing resistance to cyclobutrifluram. Additionally, point mutations H248Y in FgSdhB and A73V in FgSdhC 1 of F. graminearum were observed in the cyclobutrifluram-resistant mutants. Finally, an overexpression transformation assay and molecular docking indicated that FgSdhB H248Y or FgSdhC 1 A73V could confer resistance of F. graminearum to cyclobutrifluram., Competing Interests: Declaration of competing interest None., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Ipconazole is a broad-spectrum triazole fungicide that is highly effective against Fusarium pseudograminearum. However, its risk of developing resistance and mechanism are not well understood in F. pseudograminearum. Here, the sensitivities of 101 F. pseudograminearum isolates to ipconazole were investigated, and the average EC 50 value was 0.1072 μg/mL. Seven mutants resistant to ipconazole were obtained by fungicide adaption, with all but one showing reduced fitness relative to the parental isolates. Cross-resistance was found between ipconazole and mefentrifluconazole and tebuconazole, but none between ipconazole and pydiflumetofen, carbendazim, fludioxonil, or phenamacril. In summary, these findings suggest that there is a low risk of F. pseudograminearum developing resistance to ipconazole. Additionally, a point mutation, G464S, was seen in FpCYP51B and overexpression of FpCYP51A, FpCYP51B and FpCYP51C was observed in ipconazole-resistant mutants. Assays, including transformation and molecular docking, indicated that G464S conferred ipconazole resistance in F. pseudograminearum., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Mefentrifluconazole, a triazole fungicide, exhibits remarkable efficacy in combating Fusarium spp. The mean EC 50 value of mefentrifluconazole against 124 isolates of Fusarium pseudograminearum was determined to be 1.06 μg/mL in this study. Fungicide taming produced five mefentrifluconazole-resistant mutants with resistance factors ranging from 19.21 to 111.34. Compared to the original parental isolates, the fitness of three resistant mutants was much lower, while the remaining two mutants displayed enhanced survival fitness. There was evidence of positive cross-resistance between tebuconazole and mefentrifluconazole. Mefentrifluconazole resistance in F. pseudograminearum can be conferred by FpCYP51B L144F , which was identified in four mutants according to molecular docking and site-directed transformation experiments. Overexpression of FpCYP51s was also detected in the resistant mutants. In conclusion, mefentrifluconazole has a low-to-medium resistance risk in F. pseudograminearum , and the L144F mutation in FpCYP51B and the increased expression level of FpCYP51s may be responsible for mefentrifluconazole resistance in F. pseudograminearum .

Background: Fusarium pseudograminearum is one of the dominant pathogens of Fusarium crown rot (FCR) worldwide. Unfortunately, no fungicides have yet been registered for the control of FCR in wheat in China. Pydiflumetofen, a new-generation succinate dehydrogenase inhibitor, exhibits excellent inhibitory activity to Fusarium spp. A resistance risk assessment of F. pseudograminearum to pydiflumetofen and the resistance mechanism involved have not yet been investigated., Results: The median effective concentration (EC 50 ) value of 103 F. pseudograminearum isolates to pydiflumetofen was 0.0162 μg mL -1 , and the sensitivity exhibited a unimodal distribution. Four resistant mutants were generated by fungicide adaption, which possessed similar or impaired fitness compared to corresponding parental isolates based on the results of mycelial growth, conidiation, conidium germination rate, and virulence determination. Pydiflumetofen showed strong positive cross-resistance with cyclobutrifluram and fluopyram but no cross-resistance with carbendazim, phenamacril, tebuconazole, fludioxonil, or pyraclostrobin. Sequence alignment revealed that pydiflumetofen-resistant F. pseudograminearum mutants had two single-point mutations of A83V or R86K in FpSdhC 1 . Molecular docking further confirmed that point mutation of A83V or R86K in FpSdhC 1 could confer resistance of F. pseudograminearum to pydiflumetofen., Conclusion: Fusarium pseudograminearum shows an overall moderate risk of developing resistance to pydiflumetofen, and point mutation FpSdhC 1 A83V or FpSdhC 1 R86K could confer pydiflumetofen resistance in F. pseudograminearum. This study provided vital data for monitoring the emergence of resistance and developing resistance management strategies for pydiflumetofen. © 2023 Society of Chemical Industry., (© 2023 Society of Chemical Industry.)

Fusarium fujikuroi is one of the dominant phytopathogenic fungi causing rice bakanae disease worldwide. Cyclobutrifluram is a novel succinate dehydrogenase inhibitor (SDHI), which shows strong inhibitory activity against F. fujikuroi . The baseline sensitivity of 112 F. fujikuroi to cyclobutrifluram was determinated with a mean EC 50 value of 0.025 μg/mL. A total of 17 resistant mutants were obtained by fungicide adaptation and displayed equal or slightly weaker fitness than parental isolates, which suggests that the resistance risk of F. fujikuroi to cyclobutrifluram is medium. A positive cross-resistance was detected between cyclobutrifluram and fluopyram. The amino acid substitutions H248L/Y of FfSdhB and G80R or A83V of FfSdhC 2 conferred cyclobutrifluram resistance in F. fujikuroi , which was validated by molecular docking and protoplast transformation. The results indicate that the affinity between cyclobutrifluram and FfSdhs obviously decreased after point mutations, causing the resistance of F. fujikuroi .

Cyclobutrifluram is a novel succinate dehydrogenase inhibitor (SDHI) developed by Syngenta and helps to inhibit Fusarium pseudograminearum . Here, the potential for cyclobutrifluram resistance in F. pseudograminearum and the resistance mechanism involved were evaluated. Baseline sensitivity of F. pseudograminearum to cyclobutrifluram was determined with a mean EC 50 value of 0.0248 μg/mL. Fungicide adaption generated five resistant mutants, which possess a comparable or a slightly impaired fitness compared to corresponding parental isolates. This indicates that the resistance risk of F. pseudograminearum to cyclobutrifluram might be moderate. Cyclobutrifluram-resistant isolates also demonstrated resistance to pydiflumetofen but sensitivity to carbendazim, phenamacril, tebuconazole, fludioxonil, or pyraclostrobin. Additionally, point mutations H248Y in FpSdhB and A83V or R86K in FpSdhC 1 were found in cyclobutrifluram-resistant F. pseudograminearum mutants. Molecular docking and overexpression transformation assay revealed that FpSdhB H248Y and FpSdhC 1 A83V or FpSdhC 1 R86K confer the resistance of F. pseudograminearum to cyclobutrifluram.

Rice bakanae disease, caused by Fusarium fujikuroi, is a destructive seed-borne disease throughout the world. Prochloraz, a DMI (C-14α-demethylase inhibitor) fungicide, has been registered in China for >20 years. Prochloraz resistance in F. fujikuroi was severe in China with resistance frequencies of 34.56%, 45.33%, and 48.45% from 2019 to 2021. The fitness of prochloraz-resistant population was lower than that of sensitive population, with an average CFI of 2.86 × 10 6 and 4.56 × 10 6 , respectively. No cross-resistance was detected between prochloraz and tebuconazole or hexaconazole, and the prochloraz-resistant isolates were still sensitive to fludioxonil, phenamacril, and pydiflumetofen. S312T mutation in Ffcyp51b or overexpression of Ffcyp51a and Ffcyp51b was detected in the highly resistant isolates. AS-PCR primers were designed to detect the prochloraz-resistant isolates with S312T mutation in the field. Resistant isolates carrying S312T mutation were the dominant group in prochloraz-resistant population with frequencies of 43.26%, 23.59%, and 71.20% from 2019 to 2021, which indicated that more attention should be paid to this genotype when monitoring and managing the prochloraz resistance in F. fujikuroi., (Copyright © 2022 Elsevier Inc. All rights reserved.)

BACKGROUND: Fusarium pseudograminearum is one of the dominant pathogens of Fusarium crown rot (FCR) worldwide. Unfortunately, no fungicides have yet been registered for the control of FCR in wheat in China. Pydiflumetofen, a new‐generation succinate dehydrogenase inhibitor, exhibits excellent inhibitory activity to Fusarium spp. A resistance risk assessment of F. pseudograminearum to pydiflumetofen and the resistance mechanism involved have not yet been investigated. RESULTS: The median effective concentration (EC50) value of 103 F. pseudograminearum isolates to pydiflumetofen was 0.0162 μg mL−1, and the sensitivity exhibited a unimodal distribution. Four resistant mutants were generated by fungicide adaption, which possessed similar or impaired fitness compared to corresponding parental isolates based on the results of mycelial growth, conidiation, conidium germination rate, and virulence determination. Pydiflumetofen showed strong positive cross‐resistance with cyclobutrifluram and fluopyram but no cross‐resistance with carbendazim, phenamacril, tebuconazole, fludioxonil, or pyraclostrobin. Sequence alignment revealed that pydiflumetofen‐resistant F. pseudograminearum mutants had two single‐point mutations of A83V or R86K in FpSdhC1. Molecular docking further confirmed that point mutation of A83V or R86K in FpSdhC1 could confer resistance of F. pseudograminearum to pydiflumetofen. CONCLUSION: Fusarium pseudograminearum shows an overall moderate risk of developing resistance to pydiflumetofen, and point mutation FpSdhC1A83V or FpSdhC1R86K could confer pydiflumetofen resistance in F. pseudograminearum. This study provided vital data for monitoring the emergence of resistance and developing resistance management strategies for pydiflumetofen. © 2023 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]