Molecular and biological characterization of lab-induced benzovindiflupyr-resistant mutants of Didymella bryoniae

Wu, Zhiwen; Mao, Xuewei; Wu, Lijun; Cai, Xiaowei; Bi, Chaowei; Zhou, Mingguo; Hou, Yiping

doi:10.1016/j.cropro.2023.106260

Cited by 2 publications

(1 citation statement)

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“…Generally, reduced sensitivity to SDHI fungicides is involved with point mutations in SdhB, SdhC and SdhD subunits. 24 It is reported that SdhB H277Y mutation is involved in benzovindiflupyr resistance in Didymella bryoniae, 29 SdhB P226L and SdhD H132R refers boscalid resistance in Sclerotinia sclerotiorum, 24,30 SdhB H249Y causes thifluzamide resistance in R. solani, 17 and SdhB H267Y leads to boscalid, isopyrazam and carboxin resistance in M. graminicola. 31 In the current study, we have detected three mutations in benzovindiflupyr-resistant Sclerotium rolfsii isolates, including SdhB N180D , SdhC Q68E and SdhD H103Y .…”

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confidence: 99%

Resistance risk assessment for benzovindiflupyr in Sclerotium rolfsii and transmission of resistance genes among population

Cui,

Jiang,

Sun

et al. 2024

Pest Management Science

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BACKGROUNDSclerotium rolfsii is a destructive soil‐borne fungal pathogen which is distributed worldwide. In previous study, the succinate dehydrogenase inhibitor (SDHI) fungicide benzovindiflupyr has been identified for its great antifungal activity against S. rolfsii. This study is aimed to investigate the resistance risk and mechanism of benzovindiflupyr in S. rolfsii.RESULTSEight stable benzovindiflupyr‐resistant isolates were generated by fungicide adaptation. Although the obtained 8 resistant isolates have a stronger pathogenicity than the parental sensitive isolate, they have a fitness penalty in the mycelial growth and sclerotia formation compared to the parental isolate. A positive cross‐resistance existed in the resistant isolates between benzovindiflupyr and thifluzamide, carboxin, boscalid and isopyrazam. Three point mutations, including SdhBN180D, SdhCQ68E and SdhDH103Y, were identified in the benzovindiflupyr‐resistant isolates. However, molecular docking analysis indicated that only SdhDH103Y could influence the sensitivity of S. rolfsii to benzovindiflupyr. After mycelial co‐incubation of resistant isolates and the sensitive isolate, resistance genes may be transmitted to the sensitive isolate. The in vivo efficacy of benzovindiflupyr and thifluzamide against benzovindiflupyr‐resistant isolates was a little lower than that against the sensitive isolate but with no significant difference.CONCLUSIONAbove results suggested a low to medium resistance risk of S. rolfsii to benzovindiflupyr. However, once resistance occurs, it is possible to spread in the population of S. rolfsii. This study is helpful to understanding the risk and mechanism of resistance to benzovindiflupyr in multinucleate pathogens such as S. rolfsii.This article is protected by copyright. All rights reserved.

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