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Kartashov, M. I., Shcherbakova, L. A., Statsyuk, N. V., & Dzhavakhiya, V. G. (2019). Co-application of Difenoconazole with Thymol Results in Suppression of a Parastagonospora Nodorum Mutant Strain Resistant to this Triazole. KnE Life Sciences, 4(14), 1097–1106. https://doi.org/10.18502/kls.v4i14.5708

https://doi.org/10.18502/kls.v4i14.5708

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authors

  • M I Kartashov

    M I Kartashov

    Department of Molecular Biology, All-Russian Research Institute of Phytopathology, Bolshie Vyazemy, Russia
  • L A Shcherbakova

    L A Shcherbakova

    Laboratory of Plant Pathophysiology, All-Russian Research Institute of Phytopathology, Bolshie Vyazemy, Russia
  • N V Statsyuk

    N V Statsyuk

    Department of Potato & Vegetable Diseases, All-Russian Research Institute of Phytopathology, Bolshie Vyazemy, Russia
  • V G Dzhavakhiya

    V G Dzhavakhiya

    Department of Molecular Biology, All-Russian Research Institute of Phytopathology, Bolshie Vyazemy, Russia

Published Date

  • Nov 25, 2019

Co-application of Difenoconazole with Thymol Results in Suppression of a Parastagonospora Nodorum Mutant Strain Resistant to this Triazole

KnE Life Sciences / International Scientific and Practical Conference “AgroSMART – Smart Solutions for Agriculture” / Pages 1097–1106

Abstract

Results of in vitro study of thymol, a natural chemosensitizer, as a potential agent for overcoming of difenoconazole resistance of Parastagonospora nodorum causing glume and leaf blotch of wheat are first reported. The level of difenoconazole resistance of a natural mutant PNm1 strain with low sensitivity to the Dividend fungicide (a.i. difenoconazole) was determined by the cultivation of this isolate on potato dextrose agar in the presence of the fungicide at sub-lethal and lethal (in relation to the initial fungicide-sensitive strain) concentrations. A principal possibility of the thymol use to overcome resistance of P. nodorum to DMI (demethylation inhibitors) fungicides is shown. Co-application of this compound with Dividend SC, 3 % resulted in a significant reduction of resistance of the mutant strain and enhancement of its sensitivity to difenoconazole up to the level corresponding to the initial non-resistant isolate.

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