4.7 Article

Resistance to pydiflumetofen in Botrytis cinerea: risk assessment and detection of point mutations in sdh genes that confer resistance

Journal

PEST MANAGEMENT SCIENCE
Volume 78, Issue 4, Pages 1448-1456

Publisher

JOHN WILEY & SONS LTD
DOI: 10.1002/ps.6762

Keywords

Botrytis cinerea; pydiflumetofen; SDHI resistance; fitness

Funding

  1. Innovation Capability Support Plan of Shaanxi Province [2020TD-035]
  2. National Key Research and Development Program of China [2016YFD0201305]

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This study assessed the baseline sensitivity, resistance risk, and resistance mechanism of Botrytis cinerea to the new generation succinate dehydrogenase inhibitor pydiflumetofen. The study found resistant mutants and identified two different types of resistant mutations.
BACKGROUND Gray mold caused by Botrytis cinerea Pers. is one of the most significant airborne diseases. It can infest a wide range of crops, causing significant losses in yield and quality worldwide. Pydiflumetofen, a new generation succinate dehydrogenase inhibitor (SDHI), is currently being registered in China to control gray mold in a variety of crops. The baseline sensitivity, resistance risk, and resistance mechanism of Botrytis cinerea to pydiflumetofen were assessed in this study. RESULTS A total of 138 strains of B. cinerea from 10 different regions were tested for their sensitivity to pydiflumetofen, and the mean EC50 value was 0.0056 mu g mL(-1). Eight mutants were obtained by fungicide adaption from five sensitive parental isolates, and the resistance factor (RF) ranged from 51 to 135. The mutants exhibited strong adaptive traits in conidial production, conidial germination, and pathogenicity. Positive cross-resistance was only observed between other SDHIs (i.e. boscalid, fluopyram, and isopyrazam). Two different types of pydiflumetofen-resistant mutants were identified: point mutation P225L in sdhB and double mutation G85A and I93V in sdhC. The in vivo control efficacy of pydiflumetofen on the resistant mutants carrying P225L in sdhB as well as G85A and I93V in sdhC was significantly decreased to 52.62% and 32.27%, respectively. CONCLUSION The fitness was significantly higher for all pydiflumetofen-resistant mutants than the corresponding parental. Two types of point mutations, sdhB-P225L and sdhC-G85A and I93V, might confer resistance to pydiflumetofen in B. cinerea. A precautionary resistance management strategy should be implemented.

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