Resistance to the DMI fungicide mefentrifluconazole in Monilinia fructicola: risk assessment and resistance basis analysis

Author:

Li Guixiang1,Zhang Ling1,Wang Huakai1,Li Xiuhuan1,Cheng Fei1,Miao Jianqiang1,Peng Qin2ORCID,Liu Xili13

Affiliation:

1. State Key Laboratory for Crop Stress Resistance and High‐Efficiency Production, College of Plant Protection Northwest A&F University Yangling China

2. Key Laboratory of Plant Protection Resources and Pest Management of Ministry of Education, Key Laboratory of Integrated Pest Management on the Loess Plateau of Ministry of Agriculture and Rural Affairs, College of Plant Protection Northwest A&F University Yangling China

3. Department of Plant Pathology, College of Plant Protection China Agricultural University Beijing China

Abstract

AbstractBACKGROUNDBrown rot disease, caused by Monilinia fructicola, poses a significant challenge to peach production in China. The efficacy of mefentrifluconazole, a new triazole fungicide, in controlling brown rot in peaches has been remarkable. However, the resistance risk and mechanism associated with this fungicide remain unclear. This study was designed to assess the resistance risk of M. fructicola to mefentrifluconazole and reveal the potential resistance mechanism.RESULTSThe mean median effective concentration (EC50) of 101 M. fructicola isolates to mefentrifluconazole was 0.003 μg mL−1, and the sensitivity exhibited a unimodal distribution. Seven mefentrifluconazole‐resistant mutants were generated from three parental isolates in the laboratory through fungicide adaption. The biological characteristics of the resistant mutants revealed that three of them exhibited enhanced survival fitness compared to the parental isolates, whereas the remaining four mutants displayed reduced survival fitness. Mefentrifluconazole showed strong positive cross‐resistance with fenbuconazole, whereas no cross‐resistance was observed with pyrimethanil, procymidone or pydiflumetofen. No overexpression of MfCYP51 gene was detected in the resistant mutants. Multiple sequence alignment revealed that three resistant mutants (MXSB2‐2, Mf12‐1 and Mf12‐2) had a point mutation (G461S) in MfCYP51 protein. Molecular docking techniques confirmed the contribution of this point mutation to mefentrifluconazole resistance.CONCLUSIONThe risk of M. fructicola developing resistance to mefentrifluconazole is relatively low‐to‐medium and point mutation G461S in MfCYP51 could confer mefentrifluconazole resistance in M. fructicola. This study provided essential data for monitoring the emergence of resistance and developing resistance management strategies for mefentrifluconazole. © 2023 Society of Chemical Industry.

Funder

National Key Research and Development Program of China

Publisher

Wiley

Subject

Insect Science,Agronomy and Crop Science,General Medicine

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