Homozygous and heterozygous point mutations in succinate dehydrogenase subunits b, c and d of Rhizoctonia cerealis conferring resistance to thifluzamide

• Published in: Pest management science Vol. 73; no. 5; pp. 896 - 903
• Main Authors: Sun, Hai‐Yan, Lu, Chao‐Qun, Li, Wei, Deng, Yuan‐Yu, Chen, Huai‐Gu
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 01-05-2017; Wiley Subscription Services, Inc
• Subjects: Anilides - pharmacology; Crop diseases; Dehydrogenase; Drug Resistance, Fungal - genetics; Enzymes; Fungicides; Fungicides, Industrial - pharmacology; Heterozygote; Homozygote; homozygous and heterozygous mutation; Mutation; Pesticides; Point Mutation; Protein Subunits - genetics; Rhizoctonia - drug effects; Rhizoctonia - enzymology; Rhizoctonia - genetics; Rhizoctonia cerealis; SDHI resistance; Succinate Dehydrogenase - genetics; Thiazoles - pharmacology; thifluzamide; Triticum aestivum; Rhizoctonia cerealis; thifluzamide; SDHI resistance; homozygous and heterozygous mutation
• ISSN: 1526-498X; 1526-4998
• DOI: 10.1002/ps.4361

BACKGROUND
Thifluzamide, a succinate dehydrogenase inhibitor (SDHI) fungicide, is a promising fungicide for controlling wheat sharp eyespot (WSE). WSE is caused by Rhizoctonia cerealis. Information on the resistance mechanism of this pathogen to thifluzamide remains unavailable.
RESULTS
We used selective reculturing and UV mutagenesis to generate thifluzamide‐resistant mutants. Thifluzamide‐resistant mutants were only generated through UV mutagenesis. Sequence analysis of succinate dehydrogenase (Sdh) genes revealed that two mutants had no mutation in RCSdhB, RCSdhC and RCSdhD, and the other 18 mutants all had at least one mutation in RCSdhB, RCSdhC or RCSdhD, either in a homozygous or heterozygous state. The majority of mutants included either RCSdhD‐H116Y or RCSdhC‐H139Y. They showed slight resistance to boscalid, bixafen and penflufen. Only one mutant possessed RCSdhB‐H246Y, and it showed medium resistance to boscalid and penflufen and a slight resistance to bixafen. All the thifluzamide mutants were sensitive to flutolanil. Compared with their parental isolates, these mutants present no or minor fitness penalties.
CONCLUSION
Homozygous and heterozygous point mutations in the succinate dehydrogenase subunits b, c and d of R. cerealis may be involved in thifluzamide resistance. © 2016 Society of Chemical Industry