Induction of Fungal Resistance to Metalaxyl by Ultraviolet Irradiation

Bruin, G. C. A.

doi:10.1094/phyto-77-476

Cited by 5 publications

(6 citation statements)

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“…The ability to isolate mutants with a high level of resistance to metalaxyl in the laboratory is well documented,6–9 and our results are very similar to those of other workers. Less information is available concerning isolation in the laboratory of mutants resistant to dimethomorph than for metalaxyl.…”

Section: Discussionsupporting

confidence: 91%

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Laboratory studies to assess the risk of development of resistance to zoxamide

Young

Spiewak

Slawecki

2001

Pest Management Science

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Laboratory studies were conducted to evaluate the risk of developing field resistance to zoxamide, a new Oomycete fungicide which acts on microtubules. Zoxamide, metalaxyl and dimethomorph were compared with respect to the ease with which fungicide‐resistant mutants could be isolated and their level of resistance. Attempts to generate mutants of Phytophthora capsici and P infestans with resistance to zoxamide by mycelial adaptation on fungicide‐amended medium were unsuccessful. Similarly, changes in sensitivity to zoxamide were small (resistance factors ≤2.2) in mutants of P capsici isolated by chemical mutagenesis of zoospore cysts. In parallel experiments with metalaxyl, highly resistant mutants were obtained using both adaptation (P capsici or P infestans) and chemical mutagenesis (P capsici). For dimethomorph, chemical mutagenesis (P capsici) yielded moderately resistant mutants (maximum resistance factor = 20.9), and adaptation (P capsici or P infestans) did not induce resistance. It is proposed that failure to isolate mutants resistant to zoxamide results from the diploid nature of Oomycete fungi and the likelihood that target‐site mutations would produce a recessive phenotype. Our studies suggest that the risk of a highly resistant pathogen population developing rapidly in the field is much lower for zoxamide than for metalaxyl. However, as with any site‐specific fungicide, appropriate precautions against resistance development should be taken. © 2001 Society of Chemical Industry

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Section: Discussionsupporting

confidence: 91%

“…Field resistance to metalaxyl has been well documented,5 and various studies have shown that resistant mutants can be isolated readily in the laboratory 6–9. In the case of dimethomorph, field resistance has been reported,10 but appears rare to date.…”

Section: Introductionmentioning

confidence: 99%

Laboratory studies to assess the risk of development of resistance to zoxamide

Young

Spiewak

Slawecki

2001

Pest Management Science

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“…The sexually derived spores of oomycetes are frequently recalcitrant to germination and, for outcrossing species such as P. infestans , conversion to homozygosity requires the identification of rare lines derived from the self‐fertilization of heterozygous mutants. The mutagenesis of oomycetes to drug insensitivity has frequently led to a loss or disruption of one or more life cycle stages, pathogenicity or nutritional impairment (Bruin and Edgington, 1982; Castro et al. , 1970; Long and Keen, 1977).…”

Section: Discussionmentioning

confidence: 99%

Mandipropamid targets the cellulose synthase‐like PiCesA3 to inhibit cell wall biosynthesis in the oomycete plant pathogen, Phytophthora infestans

Blum

Boehler

Randall³

et al. 2010

Molecular Plant Pathology

120

113

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Oomycete plant pathogens cause a wide variety of economically and environmentally important plant diseases. Mandipropamid (MPD) is a carboxylic acid amide (CAA) effective against downy mildews, such as Plasmopara viticola on grapes and potato late blight caused by Phytophthora infestans. Historically, the identification of the mode of action of oomycete-specific control agents has been problematic. Here, we describe how a combination of biochemical and genetic techniques has been utilized to identify the molecular target of MPD in P. infestans. Phytophthora infestans germinating cysts treated with MPD produced swelling symptoms typical of cell wall synthesis inhibitors, and these effects were reversible after washing with H(2)O. Uptake studies with (14)C-labelled MPD showed that this oomycete control agent acts on the cell wall and does not enter the cell. Furthermore, (14)C glucose incorporation into cellulose was perturbed in the presence of MPD which, taken together, suggests that the inhibition of cellulose synthesis is the primary effect of MPD. Laboratory mutants, insensitive to MPD, were raised by ethyl methane sulphonate (EMS) mutagenesis, and gene sequence analysis of cellulose synthase genes in these mutants revealed two point mutations in the PiCesA3 gene, known to be involved in cellulose synthesis. Both mutations in the PiCesA3 gene result in a change to the same amino acid (glycine-1105) in the protein. The transformation and expression of a mutated PiCesA3 allele was carried out in a sensitive wild-type isolate to demonstrate that the mutations in PiCesA3 were responsible for the MPD insensitivity phenotype.

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“…However, pathogen genotypes that were fully insensitive to the chemical were identified soon after its widespread use (reviewed in Gisi and Sierotzki, ; Gisi et al ., ). Pathogen strains that were insensitive to Metalaxyl also exhibited cross‐resistance to other phenylamide compounds, such as Furalaxyl, Benalaxyl and Oxadixyl (Bruin and Edgington, ; Davidse et al ., ; Joseph and Coffey, ). The first reports of P. infestans field isolates insensitive to Metalaxyl originate from 1980 (Davidse et al .…”

Section: Introductionmentioning

confidence: 99%

“…Further, it is well documented that phenylamide‐insensitive laboratory mutants of Phytophthora sp. are readily generated (Bruin and Edgington, ; Davidse, ; Joseph and Coffey, ). Mefenoxam continues to be effective in controlling oomycete diseases in crops (Rebollar‐Alviter et al .…”

Section: Introductionmentioning

confidence: 99%

Sequence diversity in the large subunit of RNA polymerase I contributes to Mefenoxam insensitivity in Phytophthora infestans

Randall

Young

Sierotzki

et al. 2014

Molecular Plant Pathology

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Phenylamide fungicides have been widely used for the control of oomycete-incited plant diseases for over 30 years. Insensitivity to this chemical class of fungicide was recorded early in its usage history, but the precise protein(s) conditioning insensitivity has proven difficult to determine. To determine the genetic basis of insensitivity and to inform strategies for the cloning of the gene(s) responsible, genetic crosses were established between Mefenoxam sensitive and intermediate insensitive isolates of Phytophthora infestans, the potato late blight pathogen. F1 progeny showed the expected semi-dominant phenotypes for Mefenoxam insensitivity and suggested the involvement of multiple loci, complicating the positional cloning of the gene(s) conditioning insensitivity to Mefenoxam. Instead, a candidate gene strategy was used, based on previous observations that the primary effect of phenylamide compounds is to inhibit ribosomal RNA synthesis. The subunits of RNA polymerase I (RNApolI) were sequenced from sensitive and insensitive isolates and F1 progeny. Single nucleotide polymorphisms (SNPs) specific to insensitive field isolates were identified in the gene encoding the large subunit of RNApolI. In a survey of field isolates, SNP T1145A (Y382F) showed an 86% association with Mefenoxam insensitivity. Isolates not showing this association belonged predominantly to one P. infestans genotype. The transfer of the 'insensitive' allele of RPA190 to a sensitive isolate yielded transgenic lines that were insensitive to Mefenoxam. These results demonstrate that sequence variation in RPA190 contributes to insensitivity to Mefenoxam in P. infestans.

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Induction of Fungal Resistance to Metalaxyl by Ultraviolet Irradiation

Cited by 5 publications

References 0 publications

Laboratory studies to assess the risk of development of resistance to zoxamide

Laboratory studies to assess the risk of development of resistance to zoxamide

Mandipropamid targets the cellulose synthase‐like PiCesA3 to inhibit cell wall biosynthesis in the oomycete plant pathogen, Phytophthora infestans

Sequence diversity in the large subunit of RNA polymerase I contributes to Mefenoxam insensitivity in Phytophthora infestans

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