Laboratory mutants of Botryotinia fuckeliana resistant to the phenylpyrrole fungicide CGA 173506 were obtained from uv irradiated or non-irradiated conidia of two sensitive strains incubated on a medium containing 1 mug ml-1 active ingredient (a.i.) of the fungicide. Mutation rates, which were similar for the two parental strains, were 1.4-1.8 x 10(-4) survivors for uv-induced mutations and 2.9-9 x 10(-5) for spontaneous mutations. The mutants showed different levels of resistance to CGA 173506, and all displayed high resistance to dicarboximide fungicides. Genetic analysis of meiotic progeny of crosses between a sample of twenty mutants and reference strains showed that in most mutants resistance to CGA 173506 was caused by a single gene, which did not recombine during meiosis with the Daf1 gene responsible for resistance to dicarboximide fungicides. Mutant BAR48 proved to be a heterokaryon containing nuclei carrying mutations in the Daf1 gene, along with nuclei carrying mutations in a different gene, termed Daf2. Most laboratory mutants selected for high resistance to dicarboximides were also resistant to CGA 173506. Field isolates with low resistance to dicarboximides were, however, all normally sensitive to the phenylpyrrole fungicide.
ISOLATION, CHARACTERIZATION AND GENETIC-ANALYSIS OF LABORATORY MUTANTS OF BOTRYOTINIA-FUCKELIANA RESISTANT TO THE PHENYLPYRROLE FUNGICIDE CGA-173506
FARETRA F;POLLASTRO, Stefania
1993-01-01
Abstract
Laboratory mutants of Botryotinia fuckeliana resistant to the phenylpyrrole fungicide CGA 173506 were obtained from uv irradiated or non-irradiated conidia of two sensitive strains incubated on a medium containing 1 mug ml-1 active ingredient (a.i.) of the fungicide. Mutation rates, which were similar for the two parental strains, were 1.4-1.8 x 10(-4) survivors for uv-induced mutations and 2.9-9 x 10(-5) for spontaneous mutations. The mutants showed different levels of resistance to CGA 173506, and all displayed high resistance to dicarboximide fungicides. Genetic analysis of meiotic progeny of crosses between a sample of twenty mutants and reference strains showed that in most mutants resistance to CGA 173506 was caused by a single gene, which did not recombine during meiosis with the Daf1 gene responsible for resistance to dicarboximide fungicides. Mutant BAR48 proved to be a heterokaryon containing nuclei carrying mutations in the Daf1 gene, along with nuclei carrying mutations in a different gene, termed Daf2. Most laboratory mutants selected for high resistance to dicarboximides were also resistant to CGA 173506. Field isolates with low resistance to dicarboximides were, however, all normally sensitive to the phenylpyrrole fungicide.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
