Baseline sensitivity and action mechanism of the sterol demethylation inhibitor flusilazole to Valsa mali

2021 ◽  
Vol 171 ◽  
pp. 104722
Author(s):  
Yong Wang ◽  
Lin Jiang ◽  
Miao-Miao Wang ◽  
Jun-Tao Feng
2018 ◽  
Vol 147 ◽  
pp. 90-95 ◽  
Author(s):  
Yong Wang ◽  
Yang Sun ◽  
Zi Xiong ◽  
Kai He ◽  
Juntao Feng ◽  
...  

Plant Disease ◽  
2020 ◽  
Vol 104 (11) ◽  
pp. 2986-2993
Author(s):  
Yong Wang ◽  
Miaomaio Wang ◽  
Letian Xu ◽  
Yang Sun ◽  
Juntao Feng

In the present study, a total of 95 Botrytis cinerea single-spore strains collected from different hosts in Shaanxi Province of China were characterized for their sensitivity to the sterol demethylation inhibitor fungicide flusilazole. The effective concentration for 50% inhibition of mycelial growth (EC50) of flusilazole ranged from 0.021 to 0.372 µg/ml, with an average value of 0.093 µg/ml. Cross-resistance between flusilazole and commonly used fungicides was not detected, and no flusilazole-resistant mutants were induced. Both on detached strawberry leaves and in greenhouse experiments, flusilazole was more effective than the commonly used fungicide carbendazim at reducing gray mold. After culture on PDA plates or detached strawberry leaves, no difference in sclerotia production or pathogenicity was detected between two strains, WG12 (most sensitive to flusilazole) and MX18 (least sensitive to flusilazole). After treatment with flusilazole, however, the two strains lost the ability to produce sclerotia, and oxalic acid and ergosterol contents in mycelium decreased. Interestingly, the inhibition rate of ergosterol content in MX18 was significantly lower than that in WG12. Expression of Cyp51, BcatrD, and Bcmfs1 genes all increased after treatment with flusilazole, especially the Cyp51 and BcatrD genes. However, the expression of Cyp51 gene or BcatrD gene in WG12 and MX18 were significantly different from each other after treatment with flusilazole. In addition, no point mutations in Cyp51 gene were found in MX18. These data suggest flusilazole is a promising fungicide for resistance management of gray mold and also provided novel insights into understanding the resistance mechanism of flusilazole against plant pathogens.


2013 ◽  
Vol 66 ◽  
pp. 274-283 ◽  
Author(s):  
R.M. Beresford ◽  
P.J. Wright ◽  
P.N. Wood ◽  
N.M. Park ◽  
N.J. Larsen ◽  
...  

A survey of 41 apple orchards in Hawkes Bay (25) Nelson (7) Otago (4) and Waikato (5) provided 796 isolates of Venturia inaequalis (black spot or scab) which were tested using an agar plate assay for sensitivity to two demethylation inhibitor (DMI) fungicides (myclobutanil and penconazole) and to dodine Each fungicide was used at two concentrations to distinguish between highly sensitive sensitive and resistant isolates Sensitivity to DMIs in all regions was lower than baseline sensitivity in previous studies particularly for myclobutanil Waikato showed significantly lower DMI sensitivity than other regions Dodine sensitivity was greater than in the 1990s although Otago isolates were significantly less dodinesensitive than those from other regions In a plant inoculation assay to test control by five DMI fungicides of disease caused by resistant isolates flusilazol and difenoconazole gave significantly better disease control of resistant isolates than myclobutanil penconazole or fenbuconazole at standard field rates


2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Hao Feng ◽  
Shuai Wang ◽  
Zhaoyang Liu ◽  
Jianqiang Miao ◽  
Mingxia Zhou ◽  
...  

Abstract Pyraclostrobin, a quinone outside inhibitor (QoI) fungicide, has been registered to control apple tree Valsa canker (AVC) caused by Valsa mali in China. However, there is no data available regarding the resistance risk of V. mali to pyraclostrobin. In this study, the sensitivities of 120 V. mali isolates to pyraclostrobin were detected. The isolates were collected from apple orchards with no application of pyraclostrob at six provinces in China during 2013–2015, and showed similar sensitivity to pyraclostrobin. The EC50 values of these 120 V. mali isolates to pyraclostrobin ranged from 0.0014 to 0.0240 μg/mL, indicating an excellent inhibitory efficacy of pyraclostrobin to the pathogen. The EC50 values were distributed as a unimodal curve with a mean value of 0.0091 μg/mL, and the mean EC50 displayed correlation with geographic location. Meanwhile, three pyraclostrobin-resistant mutants (PR mutants) of V. mali were obtained using fungicide adaption method, with a resistance factor (RF) of 41.0, 56.8 and 22.0, respectively. The mutants showed a stable resistance to pyraclostrobin after 10 transfers on pyraclostrobin-free medium. Comparing with the corresponding parental isolates, the hyphal growth, mycelial dry weight and pathogenicity of PR mutants were significantly reduced, but the number of propagules showed no significant difference. More importantly, no cross-resistance of PR mutants to pyraclostrobin, tebuconazole, difenoconazole, imazalil and thiophanate-methyl was detected. In conclusion, V. mali showed a moderate risk to pyraclostrobin, and pyraclostrobin could be used as an alternative fungicide to control AVC in the field in China.


Plant Disease ◽  
2007 ◽  
Vol 91 (10) ◽  
pp. 1351-1358 ◽  
Author(s):  
T. Jobin ◽  
O. Carisse

Sensitivity of baseline and exposed populations of Venturia inaequalis to myclobutanil and to kresoxim-methyl were evaluated in vitro. For myclobutanil, the population was constructed with 238 monoconidial isolates of V. inaequalis collected from 48 orchards. For kresoxim-methyl, the population was constructed with 251 monoconidial isolates collected from 49 orchards. Baseline populations were constructed with 34 and 29 monoconidial isolates collected from apple trees that had never been treated for myclobutanil and kresoxim-methyl, respectively. Sensitivity to fungicides was evaluated based on 50% effective dose (ED50) values. The V. inaequalis population that was not exposed to myclobutanil had a baseline sensitivity (mean ED50) of 0.064 μg/ml and showed a lognormal distribution. The V. inaequalis population constructed with isolates from commercial orchards had a mean ED50 of 2.600 μg/ml, which was significantly higher than the baseline sensitivity. The distribution of ED50 values did not follow a lognormal distribution. In response to declining levels of scab control with myclobutanil and other sterol demethylation inhibitor fungicides (DMIs), three orchards were more deeply investigated. The mean ED50 values were 1.618 (n = 23), 3.079 (n = 29), and 1.500 μg/ml (n = 20) in orchards one, two, and three, respectively. Resistant isolates, according to criteria set by other studies, accounted for 39, 76, and 85% of the isolates tested. The V. inaequalis population that had never been exposed to kresoxim-methyl had a baseline sensitivity (mean ED50) of 0.092 μg/ml and showed a lognormal distribution. The V. inaequalis population constructed with isolates from commercial orchards had a mean ED50 of 6.093 μg/ml, which was significantly higher than the baseline sensitivity. The distribution of ED50 values followed a lognormal distribution. However, when a subsample of isolates was retested for their sensitivity to kresoxim-methyl with the addition of salicylhydroxamic acid (an inhibitor of alternative oxidase) at 100 μg/ml to the growth medium, more than 98% inhibition was observed for all isolates. The results from in vitro tests showed a high level of resistance to myclobutanil and a low level of resistance to kresoxim-methyl, suggesting that the use of myclobutanil and DMIs should be discontinued or significantly reduced before practical resistance is reached.


2005 ◽  
Vol 48 (2) ◽  
pp. 171-175 ◽  
Author(s):  
Hu Jianqiang ◽  
Wei Xianyong ◽  
Yao Junbing ◽  
Xie Feng ◽  
Zhu Huanqin ◽  
...  

1979 ◽  
Vol 41 (03) ◽  
pp. 475-490 ◽  
Author(s):  
Chaoho Ouyang ◽  
Che-Ming Teng

SummaryThe minimal concentration of the platelet aggregation principle (Platelet Aggregoserpen- tin, PAS) necessary to induce platelet aggregation was 10 ng/ml, about one-hundredth of that of the crude venom. PAS induced the release of platelet factors 3 and 4 from platelets, but the released platelet factor 3 was easily inactivated by the anti-phospholipid effect of PAS. Pretreatment of platelets with neuraminidase potentiated PAS-induced platelet aggregation. PAS-induced platelet aggregation was independent on released ADP; it could occur in the ADP-removing systems, such as apyrase or a combination of phosphoenolpyruvate and pyruvate kinase. However, PAS-induced platelet aggregation could be inhibited by adenine nucleotides and adenosine.PAS-induced platelet aggregation was inhibited by some anti-inflammatory agents, antimalarial drugs, local anesthetics, antihistamine and smooth muscle relaxants. After deaggregation of PAS-treated platelets, thrombin and sodium arachidonate could further induce platelet aggregation, but ADP and second dose of PAS could not. It is concluded that PAS-induced platelet aggregation is due to prostaglandin synthesis. Recent literatures on the mechanism of platelet aggregation were surveyed and the actions of PAS were discussed.


Sign in / Sign up

Export Citation Format

Share Document