Background: In 2004, field isolates of Botrytis cinerea Pers. ex Fr., resistant to strobilurin fungicides (QoIs), were first found in commercial citrus orchards in Wakayama Prefecture, Japan. Subsequently, QoI-resistant isolates of this fungus were also detected in plastic strawberry greenhouses in Saga, Ibaraki and Chiba prefectures, Japan. Biological and molecular characterisation of resistant isolates was conducted in this study.
Results: QoI-resistant isolates of B. cinerea grew well on PDA plates containing kresoxim-methyl or azoxystrobin at 1 mg L(-1), supplemented with 1 mM of n-propyl gallate, an inhibitor of alternative oxidase, whereas the growth of sensitive isolates was strongly suppressed. Results from this in vitro test were in good agreement with those of fungus inoculation tests in vivo. In resistant isolates, the mutation at amino acid position 143 of the cytochrome b gene, known to be the cause of high QoI resistance in various fungal pathogens, was found, but only occasionally. The heteroplasmy of cytochrome b gene was confirmed, and the wild-type sequence often present in the majority of resistant isolates, indicating that the proportion of mutated cytochrome b gene was very low.
Conclusion: The conventional RFLP and sequence analyses of PCR-amplified cytochrome b gene are insufficient for molecular identification of QoI resistance in B. cinerea.
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http://dx.doi.org/10.1002/ps.1773 | DOI Listing |
Microbiology (Reading)
January 2025
Department of Microbiology and Molecular Genetics, Larner College of Medicine, University of Vermont, Burlington, USA.
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Molecular Ecology and Evolution Programme, Department of Biochemistry, Genetics and Microbiology University of Pretoria Pretoria South Africa.
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January 2025
Pharmacy Department, University Clinical Hospital of Santiago de Compostela (SERGAS), 15706, Santiago de Compostela, Spain.
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January 2025
Department of Neurology, The First Affiliated Hospital of Zhengzhou University, No.1 Jianshe Dong Road, Zhengzhou, Henan, China.
Parkinson's disease (PD) and insomnia are prevalent neurological disorders, with emerging evidence implicating tryptophan (TRP) metabolism in their pathogenesis. However, the precise mechanisms by which TRP metabolism contributes to these conditions remain insufficiently elucidated. This study explores shared tryptophan metabolism-related genes (TMRGs) and molecular mechanisms underlying PD and insomnia, aiming to provide insights into their shared pathogenesis.
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