• Aspergillus nidulans;
  • Botrytis cinerea;
  • fludioxonil;
  • fungicide resistance;
  • mitotic instability

The somatic recombinogenic activity of the phenylpyrrole fungicide fludioxonil, in diploid Aspergillusnidulans was found similar to that caused by aromatic hydrocarbon and dicarboximide fungicides (AHDFs), such as iprodione, chlozolinate and tolclofos–methyl. All these fungicides not only increased the number of mitotic recombinants but also provided similar appearance, small sectors, of white and yellow mitotic recombination products. Fludioxonil highly resistant strains (resistant factor approximately 5000) of Botrytis cinerea were isolated at high frequency (1.08 × 10−5). Study of cross-resistance patterns of mutant strains to other fungicides, revealed cross-resistance of fludioxonil with dicarboximides (iprodione, procymidone, and chlozolinate) and aromatic hydrocarbons, such as tolclofos–methyl, pentachloronitrobenzene (PCNB), tecnazene and chloroneb. The positive cross-resistance relationships found between phenylpyrroles and members of the AHDFs and their ability to increase mitotic instability in diploid A.nidulans, indicate that phenylpyrroles should be included with AHDFs. A study of fitness parameters in wild-type and representative fludioxonil-resistant mutants of B. cinerea, showed that the mutation(s) leading to fludioxonil resistance may or may not affect some fitness-determining characteristics, such as sensitivity to high osmolarity, growth rate, conidial germination and germ-tube elongation. Pathogenicity tests on cucumber seedlings showed that an osmosensitive representative strain of B. cinerea, resistant to fludioxonil, was as virulent as the wild-type strain. The phenylpyrrole fungicide was ineffective, even in high concentrations, to control grey mould caused by this isolate.