SELECTION AND GENETIC ANALYSIS OF LABORATORY MUTANTS OF BOTRYOTINIA FUCKELIANA RESISTANT TO FENHEXAMID
Ten monoascosporic strains of Botryotinia fuckeliana were used in mycelium growth tests to evaluate baseline sensitivity to Fenhexamid, a fungicide recently introduced in the control of grey mould. Their response to the fungicide was EC₅₀ = 0.1-0.3 µg ml⁻¹ and MIC = 0.3-3 µg ml⁻¹. Eight laboratory m...
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description | Ten monoascosporic strains of Botryotinia fuckeliana were used in mycelium growth tests to evaluate baseline sensitivity to Fenhexamid, a fungicide recently introduced in the control of grey mould. Their response to the fungicide was EC₅₀ = 0.1-0.3 µg ml⁻¹ and MIC = 0.3-3 µg ml⁻¹. Eight laboratory mutants resistant to the fungicide were obtained from UV-irradiated or unirradiated conidia plated on Fenhexamid-amended medium (3 µg ml⁻¹). Mutation ratios were 1.7·10⁻⁶ of survivor conidia for UVinduced mutations and 0.6·10⁻⁸ for spontaneous mutations. Two levels of resistance to Fenhexamid were distinguished in mycelium growth tests: low (110 µg ml⁻¹) and high resistance (EC₅₀>100 µg ml⁻¹). In conidial germination tests, Fenhexamid proved to be a powerful inhibitor of germ tube elongation (EC₅₀ ~1 µg ml⁻¹) even for mutants displaying high resistance in mycelium tests. Resistant mutants were crossed with Fenhexamid-sensitive reference strains to derive meiotic progeny and to assess the mode of inheritance of resistant phenotypes. Segregation of resistant/sensitive phenotypes in ascospore offspring indicated that resistant phenotypes were due to mutations in single major genes inherited in Mendelian fashion and unlinked with the Mbc1 and Daf1 genes, responsible for resistance to benzimidazole and dicarboximide fungicides, respectively. |
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Their response to the fungicide was EC₅₀ = 0.1-0.3 µg ml⁻¹ and MIC = 0.3-3 µg ml⁻¹. Eight laboratory mutants resistant to the fungicide were obtained from UV-irradiated or unirradiated conidia plated on Fenhexamid-amended medium (3 µg ml⁻¹). Mutation ratios were 1.7·10⁻⁶ of survivor conidia for UVinduced mutations and 0.6·10⁻⁸ for spontaneous mutations. Two levels of resistance to Fenhexamid were distinguished in mycelium growth tests: low (1<EC₅₀>10 µg ml⁻¹) and high resistance (EC₅₀>100 µg ml⁻¹). In conidial germination tests, Fenhexamid proved to be a powerful inhibitor of germ tube elongation (EC₅₀ ~1 µg ml⁻¹) even for mutants displaying high resistance in mycelium tests. Resistant mutants were crossed with Fenhexamid-sensitive reference strains to derive meiotic progeny and to assess the mode of inheritance of resistant phenotypes. Segregation of resistant/sensitive phenotypes in ascospore offspring indicated that resistant phenotypes were due to mutations in single major genes inherited in Mendelian fashion and unlinked with the Mbc1 and Daf1 genes, responsible for resistance to benzimidazole and dicarboximide fungicides, respectively.</description><identifier>ISSN: 1125-4653</identifier><identifier>EISSN: 2239-7264</identifier><language>eng</language><publisher>An International Journal of the Italian Phytopathological Society</publisher><subject>Ascospores ; Benzimidazoles ; Botryotinia fuckeliana ; Botrytis ; Conidia ; Fungicides ; Genetic mutation ; Medical genetics ; Microbial genetics ; Phenotypes ; Phytopathology</subject><ispartof>Journal of plant pathology, 2007-07, Vol.89 (2), p.203-210</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/41998379$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/41998379$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>315,781,785,804,58022,58255</link.rule.ids></links><search><creatorcontrib>De Guido, M.A.</creatorcontrib><creatorcontrib>De Miccolis Angelini, R.M.</creatorcontrib><creatorcontrib>Pollastro, S.</creatorcontrib><creatorcontrib>Santomauro, A.</creatorcontrib><creatorcontrib>Faretra, F.</creatorcontrib><title>SELECTION AND GENETIC ANALYSIS OF LABORATORY MUTANTS OF BOTRYOTINIA FUCKELIANA RESISTANT TO FENHEXAMID</title><title>Journal of plant pathology</title><description>Ten monoascosporic strains of Botryotinia fuckeliana were used in mycelium growth tests to evaluate baseline sensitivity to Fenhexamid, a fungicide recently introduced in the control of grey mould. Their response to the fungicide was EC₅₀ = 0.1-0.3 µg ml⁻¹ and MIC = 0.3-3 µg ml⁻¹. Eight laboratory mutants resistant to the fungicide were obtained from UV-irradiated or unirradiated conidia plated on Fenhexamid-amended medium (3 µg ml⁻¹). Mutation ratios were 1.7·10⁻⁶ of survivor conidia for UVinduced mutations and 0.6·10⁻⁸ for spontaneous mutations. Two levels of resistance to Fenhexamid were distinguished in mycelium growth tests: low (1<EC₅₀>10 µg ml⁻¹) and high resistance (EC₅₀>100 µg ml⁻¹). In conidial germination tests, Fenhexamid proved to be a powerful inhibitor of germ tube elongation (EC₅₀ ~1 µg ml⁻¹) even for mutants displaying high resistance in mycelium tests. Resistant mutants were crossed with Fenhexamid-sensitive reference strains to derive meiotic progeny and to assess the mode of inheritance of resistant phenotypes. Segregation of resistant/sensitive phenotypes in ascospore offspring indicated that resistant phenotypes were due to mutations in single major genes inherited in Mendelian fashion and unlinked with the Mbc1 and Daf1 genes, responsible for resistance to benzimidazole and dicarboximide fungicides, respectively.</description><subject>Ascospores</subject><subject>Benzimidazoles</subject><subject>Botryotinia fuckeliana</subject><subject>Botrytis</subject><subject>Conidia</subject><subject>Fungicides</subject><subject>Genetic mutation</subject><subject>Medical genetics</subject><subject>Microbial genetics</subject><subject>Phenotypes</subject><subject>Phytopathology</subject><issn>1125-4653</issn><issn>2239-7264</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNotjE9rwjAAxcPYYM7tIwxy2q2Q5l-bY6yphtUGaoR5Km2agqLTNXrYt183d3nv8fi9dwcmGBMRJZjTezCJY8wiyhl5BE8h7BGiLEF8Avq1KlRmtSmhLOdwoUpldTZmWWzXeg1NDgs5M5W0ptrC1cbK0v61M2OrrbG61BLmm-xdFXocwUqNq18IWgNzVS7Vh1zp-TN46JtD8C__PgWbXNlsGRVmoTNZRHuM0kskGKWedz3pXOtd63zCUt56lratH5UI2iEsWOyE954njOOm6zvXEO8Fc3FDpuDt9nseTl9XHy71cRecPxyaT3-6hhojzAVCZARfb-A-XE5DfR52x2b4rmksREoSQX4AjklXJg</recordid><startdate>20070701</startdate><enddate>20070701</enddate><creator>De Guido, M.A.</creator><creator>De Miccolis Angelini, R.M.</creator><creator>Pollastro, S.</creator><creator>Santomauro, A.</creator><creator>Faretra, F.</creator><general>An International Journal of the Italian Phytopathological Society</general><scope>8FD</scope><scope>FR3</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20070701</creationdate><title>SELECTION AND GENETIC ANALYSIS OF LABORATORY MUTANTS OF BOTRYOTINIA FUCKELIANA RESISTANT TO FENHEXAMID</title><author>De Guido, M.A. ; De Miccolis Angelini, R.M. ; Pollastro, S. ; Santomauro, A. ; Faretra, F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j208t-9544e6df3dcbecbce7586be58bbee58394d02951c9eee67562adfdca3ee95c1a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Ascospores</topic><topic>Benzimidazoles</topic><topic>Botryotinia fuckeliana</topic><topic>Botrytis</topic><topic>Conidia</topic><topic>Fungicides</topic><topic>Genetic mutation</topic><topic>Medical genetics</topic><topic>Microbial genetics</topic><topic>Phenotypes</topic><topic>Phytopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>De Guido, M.A.</creatorcontrib><creatorcontrib>De Miccolis Angelini, R.M.</creatorcontrib><creatorcontrib>Pollastro, S.</creatorcontrib><creatorcontrib>Santomauro, A.</creatorcontrib><creatorcontrib>Faretra, F.</creatorcontrib><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Journal of plant pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>De Guido, M.A.</au><au>De Miccolis Angelini, R.M.</au><au>Pollastro, S.</au><au>Santomauro, A.</au><au>Faretra, F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SELECTION AND GENETIC ANALYSIS OF LABORATORY MUTANTS OF BOTRYOTINIA FUCKELIANA RESISTANT TO FENHEXAMID</atitle><jtitle>Journal of plant pathology</jtitle><date>2007-07-01</date><risdate>2007</risdate><volume>89</volume><issue>2</issue><spage>203</spage><epage>210</epage><pages>203-210</pages><issn>1125-4653</issn><eissn>2239-7264</eissn><abstract>Ten monoascosporic strains of Botryotinia fuckeliana were used in mycelium growth tests to evaluate baseline sensitivity to Fenhexamid, a fungicide recently introduced in the control of grey mould. Their response to the fungicide was EC₅₀ = 0.1-0.3 µg ml⁻¹ and MIC = 0.3-3 µg ml⁻¹. Eight laboratory mutants resistant to the fungicide were obtained from UV-irradiated or unirradiated conidia plated on Fenhexamid-amended medium (3 µg ml⁻¹). Mutation ratios were 1.7·10⁻⁶ of survivor conidia for UVinduced mutations and 0.6·10⁻⁸ for spontaneous mutations. Two levels of resistance to Fenhexamid were distinguished in mycelium growth tests: low (1<EC₅₀>10 µg ml⁻¹) and high resistance (EC₅₀>100 µg ml⁻¹). In conidial germination tests, Fenhexamid proved to be a powerful inhibitor of germ tube elongation (EC₅₀ ~1 µg ml⁻¹) even for mutants displaying high resistance in mycelium tests. Resistant mutants were crossed with Fenhexamid-sensitive reference strains to derive meiotic progeny and to assess the mode of inheritance of resistant phenotypes. Segregation of resistant/sensitive phenotypes in ascospore offspring indicated that resistant phenotypes were due to mutations in single major genes inherited in Mendelian fashion and unlinked with the Mbc1 and Daf1 genes, responsible for resistance to benzimidazole and dicarboximide fungicides, respectively.</abstract><pub>An International Journal of the Italian Phytopathological Society</pub><tpages>8</tpages></addata></record> |
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subjects | Ascospores Benzimidazoles Botryotinia fuckeliana Botrytis Conidia Fungicides Genetic mutation Medical genetics Microbial genetics Phenotypes Phytopathology |
title | SELECTION AND GENETIC ANALYSIS OF LABORATORY MUTANTS OF BOTRYOTINIA FUCKELIANA RESISTANT TO FENHEXAMID |
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