Open AccessMolecular mechanism of resistance of Fusarium fujikuroi to benzimidazole fungicides
Author(s) -
Chen Zihao,
Gao Tao,
Liang Shuping,
Liu Kexue,
Zhou Mingguo,
Chen Changjun
Publication year - 2014
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/1574-6968.12504
Subject(s) - carbendazim , biology , fungicide , mutant , genetics , gene , microbiology and biotechnology , botany
Although carbendazim ( MBC ) and other benzimidazole fungicides have effectively controlled bakanae disease of rice (which is caused by Fusarium fujikuroi , F. proliferatum , and F. verticillioides ) in the past, MBC resistance has become common. Previous research has shown that MBC resistance results from a mutation in the β 1 ‐tubulin ( β 1 tub ) gene in F. verticillioides . However, MBC resistance in F. fujikuroi , a predominant species in China, does not result from a mutation in the β 1 tub . The molecular mechanism of F. fujikuroi resistance against benzimidazole fungicides is poorly understood. In this study, we determined that although β 1 tub and β 2 ‐tubulin ( β 2 tub ) in F. fujikuroi have high homology with β 1 tub and β 2 tub in F. verticillioides , MBC resistance in F. fujikuroi results from mutations in β 2 tub [ GAG (Glu)→ GTG (Val) at codon 198, TTC (Phe)→ TAC (Tyr) at codon 200, and GGC (Gly)→ GGT (Gly) at codon 235] but not in β 1 tub . Δ β 2 tub ( β 2 tub deletion) mutants were highly sensitive to MBC , produced fewer conidia and were less virulent than parental strains. Complementation of the Δ β 2 tub mutants with a copy of the whole β 2 tub locus from their parental strains restored the level of MBC resistance (or sensitivity) to that of the parental strain.