Reduced sensitivity of <i>Cercospora beticola</i> isolates to sterol‐demethylation‐inhibiting fungicides

Karaoglanidis, G. S.; Ioannidis, P. M.; Thanassoulopoulos, C. C.

doi:10.1046/j.1365-3059.2000.00488.x

Cited by 93 publications

(51 citation statements)

References 18 publications

(20 reference statements)

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“…Experimental designs must allow for measurement of immigration of sensitive or resistant individuals from neighbouring crops. Although monitoring a mixture of azoxystrobin resistant and sensitive isolates of Magnaporthe oryzae inoculated on ryegrass Lolium perenne (Ma & Uddin 2009), and the frequency of azole resistance in Cercospora beticola during an epidemic (Karaoglanidis et al 2001), both indicated a fitness penalty linked to resistance. In general, many similar studies have not found a significant fitness penalty associated with resistance (e.g.…”

Section: Managing Resistance In Cropsmentioning

confidence: 99%

Fungicide resistance: facing the challenge - a review

Hollomon¹

2015

Plant Prot. Sci.

129

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Hollomon D.W. (2015): Fungicide resistance: facing the challenge. Plant Protect. Sci., Fungicide resistance continues to generate disease control problems in many crops. Experience amassed over the past fifty years has emphasised the importance of diversity in modes of action in anti-resistance strategies. Because of losses, not only from resistance, but increasingly from environmental and health concerns, the number of modes of action has become dangerously small. This paper considers three challenges facing crop protection in the search for durable disease control systems. Greater understanding of the biochemistry surrounding fungal development and pathogenicity provides opportunities for the discovery and development of novel modes of action, and some recent advances in this area are discussed. To ensure sufficient resources available to take a novel discovery forward to a commercial product, a second challenge facing manufacturers involves early assessment of resistance risk. A third challenge facing researchers, manufacturers and growers requires translation of resistance risk into effective and durable disease control strategies in actual crops. At the core of this challenge is using resistance risk evidence obtained in laboratory and glasshouse studies using individual isolates of target pathogens, to evaluate the fitness cost of resistance in pathogen populations in field crops. Increasingly, management of resistance is seen as the integration of fungicides with non-chemical disease control methods. But success of any Integrated Disease Management (IDM) strategy ultimately depends on the ability of growers to maintain production and profitability.

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Section: Managing Resistance In Cropsmentioning

confidence: 99%

Fungicide resistance: facing the challenge - a review

Hollomon¹

2015

Plant Prot. Sci.

129

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“…Isolates resistant to the benzimidazoles appeared in the early of 1970s resulting in complete failure of disease control (Georgopoulos and Dovas, 1973;Weiland and Halloin, 2001). The replacement of benzimidazoles with the triazole fungicides was only a temporary solution to the problem because in the last 10 years triazole-resistant isolates were also reported (Karaoglanidis et al, 2000). The organotin fungicide fentin-acetate, which was used in the anti-resistance strategies was withdrawn and the use of the dithiocarbamate maneb may eventually be restricted.…”

Section: Introductionmentioning

confidence: 99%

Biological and molecular characterization of laboratory mutants of Cercospora beticola resistant to Qo inhibitors

et al. 2006

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The resistance to strobilurin-related fungicides and its molecular basis in laboratory mutant isolates of Cercospora beticola was investigated. After ultraviolet mutagenesis, mutants with high, moderate or low resistance levels to pyraclostrobin were isolated from a wild-type strain of C. beticola. Fungitoxicity tests on the response of resistant isolates on medium containing pyraclostrobin and salicylhydroxamate (SHAM), a specific inhibitor of cyanide-resistant (alternative) respiration, indicated that the biochemical mechanism of alternative oxidase was not responsible for the reduced sensitivity to pyraclostrobin for half of the mutants. Cross-resistance studies with other inhibitors of the cytochrome bc 1 complex of the mitochondrial respiratory chain showed that the mutation(s) for resistance to pyraclostrobin also reduced the sensitivity of mutant strains to other Qo inhibitors such as azoxystrobin and fenamidone, but not to the Qi inhibitor cyazofamid. No effect of pyraclostrobin-resistant mutation(s) on fungitoxicity of the carboxamide boscalid, the triazoles epoxiconazole and flutriafol and to the benzimidazole benomyl, which affect other cellular pathways or other steps of the respiratory chain, was observed. Study of fitness parameters showed that most mutants had a significant reduction in sporulation and pathogenicity compared to the wild-type parental isolate. However, experiments on the stability of the resistant phenotype did not show a significant reduction of the resistance for half of the mutants when grown for at least four generations on pyraclostrobin-free medium. Molecular analysis of cytochrome b cDNA, isolated from the wild-type and the pyraclostrobin-resistant mutant isolates, revealed two novel amino acid replacements at positions involved in Qo resistance in other species. The glycine (GGT) to serine (AGT) replacement at position 143 (G143S) was found in the isolate with the highly resistant phenotype. The second amino acid change was the replacement of phenylalanine (TTC) by valine (GTC) at position 129 (F129V), which was found in a mutant strain with the moderately resistant phenotype. Four additional mutations located in conserved regions of the mitochondrial cytochrome b gene (I154L, N250D, E256G and V261D) were detected in some mutant isolates of C. beticola but their possible role in Qo-resistance needs further investigation. This is the first study reporting C. beticola strains resistant to Qo inhibitor fungicides due to the biochemical mechanism of target-site modification, resulting from amino acid changes in the mitochondrial cytochrome b gene.

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“…Resistance has been reported in other growing regions (Karaoglanidis et al, 2000, Secor et al, 2010, Trkulja et al, 2015. Field resistance of C. beticola to DMI fungicides poses a challenge for sugar beet production in Ontario due to favourable conditions for disease and the presence of QoI-insensitive C. beticola in the same growing region (Trueman et al, 2013), leaving copper and ethylene bisdithiocarbamate fungicides as the only effective tools for disease management.…”

Section: Figurementioning

confidence: 99%