Mechanism of Resistance to Fungicides

Hollomon, D. W.; Butters, J. A.; Kendall, S. J.

doi:10.1007/978-3-662-03458-3_1

Cited by 9 publications

(8 citation statements)

References 41 publications

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“…35 However, even in this apparently straightforward case it would have been difficult to predict that of the four regions of the b-tubulin gene that can mutate to give benzimidazole resistance in the laboratory, only mutants from one region, 196È200, are found in the Ðeld. 16 A similar divergence between laboratory mutants and Ðeld mutants has been seen with resistance to the dicarboximides in B. cinerea. In both laboratory and Ðeld mutants, resistance is determined by a single polymorphic major gene34 but the laboratory mutant phenotype (genotype Daf1HR) with high resistance factors, lower Ðtness (osmotic sensitivity) and crossresistance to the unrelated phenylpyrrole fungicides has never been detected in the Ðeld.…”

Section: Resistant Mutantsmentioning

confidence: 73%

Pesticide resistance: assessment of risk and the development and implementation of effective management strategies†

Jutsum¹,

Heaney²,

Perrin³

et al. 1998

Pestic. Sci.

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: Insecticides, fungicides and herbicides are critical to successful crop production, but the development of pesticide resistance is a continual threat, especially to many of todayÏs selective toxophores with speciÐc binding sites. In order to manage resistance e †ectively, an assessment of genetic, ecological and operational risk factors is required, which must then be translated into meaningful local strategies that can be implemented through appropriate labelling of products and education of end users. Assessing resistance risk is a fundamental part of the development process for new molecules and is increasingly becoming a requirement of registration alongside toxicological and environmental risk data. Laboratory studies, including elucidation of target sites and metabolic degradation pathways, mutagenesis, computer models and cross-resistance tests, and Ðeld studies, including establishment of baseline sensitivities and evaluation of anti-resistance strategies, all play a part in such assessment. The challenge is then to devise management strategies which are relevant to local practice and actually reduce selection pressure to a point where product life is preserved. A preventative strategy should be in place at time of launch and for most pesticides, regional co-operation between all interested parties, of the kind advocated by the Resistance Action Committees of GCPF (Global Crop Protection Federation), increases the chance of success. Implementation of strategies via a universal product labelling system, already practised in some herbicide markets, is seen as a key way to improve product usage patterns. Monitoring resistance levels in Ðeld populations after product launch enables any Ðne tuning of tactics over time, for example in response to new technologies such as transgenic varieties being introduced. The limited successes in resistance management in Australia, Zimbabwe, Europe and USA are not so easily achieved in small-holder farming in developing countries, as exempliÐed by continuing problems in parts of India and China. Emphasis must be given to the education of growers and dealers in IRM and IPM, and improved extension services, in order to bring about a more sustainable approach to crop protection.1998 Society of Chemical Industry ( Pestic. Sci., 54, 435È446 (1998)

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Section: Resistant Mutantsmentioning

confidence: 73%

Pesticide resistance: assessment of risk and the development and implementation of effective management strategies†

Jutsum¹,

Heaney²,

Perrin³

et al. 1998

Pestic. Sci.

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“…1b,d). Quinoxyfen had no activity against Bgh once the primary appressorium had formed and the pathogen had penetrated the host (Hollomon et al ., 1997a,b). Quinoxyfen resistant isolates showed an abnormal production of conidiophores and conidia (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…5, lane 7). At this point NTG1 was producing conidiophore‐like structures that failed to differentiate conidia (Hollomon et al ., 1997a,b). This experiment was repeated and, although not all time‐points were included, it confirmed that the Gap gene was expressed in the resistant mutant NTG1 in the later stages of the infection process but not in the conidia.…”

Section: Resultsmentioning

confidence: 99%

“…hordei (isolate 23D5), was collected in the early 1970s, before the widespread use of fungicides, and was the wild‐type standard. Quinoxyfen‐resistant mutants were generated from isolate 23D5 by chemical mutagenesis with N‐methyl‐N′ nitro N‐nitrosoguanidine (NTG, Hollomon et al ., 1997a,b). The work described here considered one mutant, NTG1, in detail, but alludes to mutants NTG2 and 25T in the DD‐RTPCR work.…”

Section: Methodsmentioning

confidence: 99%

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Quinoxyfen perturbs signal transduction in barley powdery mildew (Blumeria graminis f.sp. hordei)

Wheeler

Hollomon

Gustafson³

et al. 2003

Molecular Plant Pathology

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SUMMARY Quinoxyfen is a protectant fungicide which controls powdery mildew diseases by interfering with germination and/or appressorium formation. Mutants of barley powdery mildew, Blumeria graminis f.sp. hordei, which are resistant to quinoxyfen produce fewer conidia, which germinate and form appressoria more promiscuously than do the prolific numbers of wild‐type spores. This suggests that resistance bypasses host recognition signals. RT‐PCR profiles of signal transduction genes, recorded during wild‐type germling morphogenesis, reveals that quinoxyfen alters the accumulation of Protein Kinase C (pkc), pkc‐like and catalytic subunit of Protein Kinase A (cpka) transcripts. Differential display‐reverse transcription PCR identified a gene transcript in wild‐type conidia that was absent, or much less abundant, in conidia from quinoxyfen‐resistant mutants. This mRNA was not detectable 24 h after wild‐type conidia were inoculated on to barley. It encodes a GTPase activating protein (GAP), which may interact with a small molecular weight Ras‐type GTP binding protein. In the presence of quinoxyfen, the gap mRNA remains throughout germling morphogenesis. The involvement of GAP in resistance suggests that quinoxyfen inhibits mildew infection by disrupting early cell signalling events.

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“…Raramente isso ocorre, mas se dá quando a resistência se torna um problema prático e a população não mutante original pode precisar de anos para se restabelecer (HOLLOMON, 1997). Alterações que ocorrem nas espécies mutantes são conhecidas no caso dos fungicidas do grupo químico dos benzimidazóis, DMI (triazóis) e estrobilurinas (DAVIDSE; ISHII, 1995;DELYE et al, 1998;KOELLER, 1999;GISI et al,2000;SIEROTSKI et al, 2000).…”

Section: Resistênciaunclassified

Caracterização da resistência a fungicidas em populações de fungos associados a lesões de Sigatokas em bananais do Vale do Ribeira (SP)

Malipensa¹

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Mechanism of Resistance to Fungicides

Cited by 9 publications

References 41 publications

Pesticide resistance: assessment of risk and the development and implementation of effective management strategies†

Pesticide resistance: assessment of risk and the development and implementation of effective management strategies†

Quinoxyfen perturbs signal transduction in barley powdery mildew (Blumeria graminis f.sp. hordei)

Caracterização da resistência a fungicidas em populações de fungos associados a lesões de Sigatokas em bananais do Vale do Ribeira (SP)

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