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Resistance to 3,5‐dichlorophenyl‐N‐cyclic imide (‘dicarboximide’) fungicides in the grey mould pathogen Botrytis cinerea on protected crops
Year:
1982
Source of publication :
Plant Pathology
Authors :
Katan, Talma
;
.
Volume :
31
Co-Authors:

KATAN, T., Division of Plant Pathology, Agricultural Research Organization, The Volcani Center, P.O. Box 6, Bet Dagan, 50250, Israel

Facilitators :
From page:
133
To page:
141
(
Total pages:
9
)
Abstract:
Spores of laboratory isolates of Botrytis cinerca did not germinate on potato‐dextrose agar (PDA) containing 5 μg/ml dicarboximide fungicides (iprodione, vinclozolin, procymidone, Serinal, Co 4462, Co 6054). Spores from diseased cucumbers, tomatoes, strawberries and eggplants, from greenhouses where iprodione and vinclozolin failed to control grey mould, germinated normally on PDA containing 100 μg/ml vinclozolin. The fungicide concentrations that reduced the mycelial growth rate of these resistant strains by 50% ranged from 1‐0 to 4‐9 μg/ml for six dicarboximides and dicloran. These values were between nine and 26 times greater than the values for sensitive strains (0.10‐0.27 μg/ml). Mycelial growth of resistant strains was inhibited at lower fungicide concentrations than was spore germination. On average, resistant strains grew 25‐30% slower than sensitive strains. Dicarboximide‐resistant strains were all resistant to benomyl but sensitive to prochloraz. Of 37 resistant strains transferred four to 19 times on fungicide‐free PDA, 36 were stable in their resistance. In four in vivo systems, various plant parts were treated with dicarboximide fungicides (500–2500 μg/ml) and then inoculated with mycelial plugs. Protection was observed against sensitive strains of B. cinerea but not against dicarboximide‐resistant strains. Lesion development of resistant strains was often slower than that of sensitive strains. The emergence of resistant strains apparently resulted from selection pressure imposed on the pathogen population by exclusive and extensive use of dicarboximides under conditions favouring grey mould epidemics on protected crops. Copyright © 1982, Wiley Blackwell. All rights reserved
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DOI :
10.1111/j.1365-3059.1982.tb02821.x
Article number:
0
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
21671
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:45
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Scientific Publication
Resistance to 3,5‐dichlorophenyl‐N‐cyclic imide (‘dicarboximide’) fungicides in the grey mould pathogen Botrytis cinerea on protected crops
31

KATAN, T., Division of Plant Pathology, Agricultural Research Organization, The Volcani Center, P.O. Box 6, Bet Dagan, 50250, Israel

Resistance to 3,5‐dichlorophenyl‐N‐cyclic imide (‘dicarboximide’) fungicides in the grey mould pathogen Botrytis cinerea on protected crops
Spores of laboratory isolates of Botrytis cinerca did not germinate on potato‐dextrose agar (PDA) containing 5 μg/ml dicarboximide fungicides (iprodione, vinclozolin, procymidone, Serinal, Co 4462, Co 6054). Spores from diseased cucumbers, tomatoes, strawberries and eggplants, from greenhouses where iprodione and vinclozolin failed to control grey mould, germinated normally on PDA containing 100 μg/ml vinclozolin. The fungicide concentrations that reduced the mycelial growth rate of these resistant strains by 50% ranged from 1‐0 to 4‐9 μg/ml for six dicarboximides and dicloran. These values were between nine and 26 times greater than the values for sensitive strains (0.10‐0.27 μg/ml). Mycelial growth of resistant strains was inhibited at lower fungicide concentrations than was spore germination. On average, resistant strains grew 25‐30% slower than sensitive strains. Dicarboximide‐resistant strains were all resistant to benomyl but sensitive to prochloraz. Of 37 resistant strains transferred four to 19 times on fungicide‐free PDA, 36 were stable in their resistance. In four in vivo systems, various plant parts were treated with dicarboximide fungicides (500–2500 μg/ml) and then inoculated with mycelial plugs. Protection was observed against sensitive strains of B. cinerea but not against dicarboximide‐resistant strains. Lesion development of resistant strains was often slower than that of sensitive strains. The emergence of resistant strains apparently resulted from selection pressure imposed on the pathogen population by exclusive and extensive use of dicarboximides under conditions favouring grey mould epidemics on protected crops. Copyright © 1982, Wiley Blackwell. All rights reserved
Scientific Publication
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