Mode of Action and Genetic Analysis of Resistance to Fluazinam in Ustilago maydis

Abstract

Ustilago maydis strains, with low to moderate resistance to fluazinam (Rf ranging from 11.8 to 80), were isolated in a mutation frequency of 0.75 × 10−7 after chemical mutagenesis with N‐methyl‐N‐nitro‐N‐nitrosoguanidine (MNNG). Genetic analysis resulted in the identification of two chromosomal genes. A study of the effect of mutant genes in the phytopathogenic fitness of U. maydis revealed that the resistance mutations had no apparent effect on mycelia growth rate and pathogenicity on young corn plants. Cross‐resistant studies showed that the mutations for resistance to fluazinam were also responsible for resistance to oligomycin, but not to dinitrophenol. A dose‐dependent inhibition of glucose oxidation in whole cells was observed by both fluazinam and oligomycin, and a complete inhibition was found at 40 μg/ml. The results obtained provide strong evidence that the mode of action of fluazinam consists of the inhibition the fungal cell's energy production process through direct inhibition of the ATP synthetase.

Sensitivity to boscalid in field isolates of Sclerotinia sclerotiorum from rapeseed in Henan Province, China

“…The reason is that the mechanism of action of boscalid is different with those fungicides. The mode of action of the benzimidazole fungicide carbendazim, the dicarboximide fungicides procymidone, iprodione and dimethachlone, the phenylpyrrole fungicide fludioxonil and the dinitroaniline fungicide fluazinam was to inhibit the assembly of microtubules by binding to beta-tubulin (Liu, Duan, Ge, Chen, & Zhou, 2013;Liu et al, 2010;Zhu et al, 2016), the two-component histidine kinase activity (Dry, Yuan, & Hutton, 2004;Ma, Yan, Luo, & Michailides, 2007;Oshima et al, 2006), split protein kinase/histidine kinase active (Leroux, 1996;Liu et al, 2017;Zhao, Kim, Huang, & Xiao, 2010) and uncoupling of mitochondrial oxidative phosphorylation and inhibition of ATP synthase (Cross & Müller, 2004;Liang, Di, Li, & Zhu, 2015;Vitoratos, 2014;Wang, Duan, & Zhou, 2016), respectively.…”

Control of white mold of dry bean and residual activity of fungicides applied by chemigation

“…Fluazinam is considered a protectant (Lemay et al, 2002;Vitoratos, 2014) and must be applied prior to disease onset for best results, which typically coincides with first bloom and an additional application may be necessary if the favorable conditions to white mold continues (Paula Júnior et al, 2009b). The mode of action of fluazinam is uncoupling of mitochondrial oxidative phosphorylation, consequently halting synthesis of ATP without affecting the respiratory chain and ATP synthesis (Guo et al, 1991;Vitoratos, 2014). With activity at multiple sites, fluazinam is considered to have a low risk of resistance development (Lehner et al, 2015).…”

Dissipation of fluazinam in citrus groves and a risk assessment for its dietary intake

“…) is a preventative dinitroaniline fungicide with high activity. The mechanism of action of fluazinam is to inhibit ATP synthase directly by uncoupling oxidative phosphorylation . In China, fluazinam has been registered for the control of various diseases in crops such as potato, pepper, apple, Chinese cabbage, tomato, citrus, cucumber, apple, ginseng, rice, and rape.…”

“…The mechanism of action of fluazinam is to inhibit ATP synthase directly by uncoupling oxidative phosphorylation. 7,8 In China, fluazinam has been registered for the control of various diseases in crops such as potato, pepper, apple, Chinese cabbage, tomato, citrus, cucumber, apple, ginseng, rice, and rape. Some studies have reported that fluazinam has good efficacy against citrus anthracnose (http://www.chinapesticide.org.cn/yxcftozwf.jhtml).…”