scholarly journals Fungicide resistance of Cercospora beticola isolates collected from Wielkopolska region

2013 ◽  
Vol 53 (4) ◽  
Keyword(s):  
Fungicide Resistance ◽  
Cercospora Beticola

MOLECULAR BASIS OF FUNGICIDE RESISTANCE IN CERCOSPORA BETICOLA

2013 ◽  
Author(s):  
Melvin D. Bolton ◽  
Gary A. Secor ◽  
Viviana Rivera-Varas ◽  
Mohamed F. R. Khan
Keyword(s):  
Fungicide Resistance ◽  
Molecular Basis ◽  
Cercospora Beticola

scholarly journals Monitoring and managing fungicide resistance using the Cercospora beticola model

2013 ◽  
Author(s):  
Gary Secor ◽  
Viviana Rivera-Varas ◽  
Melvin Bolton ◽  
Mohamed Khan
Keyword(s):  
Fungicide Resistance ◽  
Cercospora Beticola

scholarly journals Use of PCR-RFLP Analysis to Monitor Fungicide Resistance in Cercospora beticola Populations from Sugarbeet (Beta vulgaris) in Michigan, United States

Plant Disease ◽  
2015 ◽  
Vol 99 (3) ◽  
pp. 355-362 ◽  
Author(s):  
N. Rosenzweig ◽  
L. E. Hanson ◽  
G. Clark ◽  
G. D. Franc ◽  
W. L. Stump ◽  
...  
Keyword(s):  
Beta Vulgaris ◽  
Cytochrome B ◽  
Fungicide Resistance ◽  
Cercospora Beticola ◽  
Benzimidazole Fungicides ◽  
Mitochondrial Cytochrome B ◽  
Standard Polymerase Chain Reaction ◽  
Field Samples ◽  
Pcr Rflp ◽  
Β Tubulin

Genetic resistance to Quinone outside inhibitor (QoI) and benzimidazole fungicides may be responsible for a recent decline in efficacy of chemical control management strategies for Cercospora leaf spot (CLS) caused by Cercospora beticola in Michigan sugarbeet (Beta vulgaris) fields. The target genes and fungicide resistance mutations are known for these two fungicides. Based on this, two standard polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) assays were developed to detect the G143A and E198A point mutations in the fungal mitochondrial cytochrome b and the β-tubulin genes, respectively. These mutations confer a high level of resistance to either QoI or benzimidazole fungicides. The presence of the G143A and E198A mutations was monitored within C. beticola populations recovered from Michigan sugarbeet production fields collected in 2012. Both the QoI-resistant cytochrome b allele and the benzimidazole-resistant β-tubulin allele were detected directly from leaf tissue following a PCR-RFLP assay. Using either detection assay, the G143A and E198A mutations were detected in over 90% of the 118 field samples originating from Michigan sugarbeet production under fungicide management programs for CLS control. Monitoring of the G143A and E198A mutations in fields located in 9 counties and 58 townships indicated that the mutations were widespread in Michigan sugarbeet production areas. The PCR-based assays used and developed in this study were effective in detecting the presence of the G143A and E198A mutations in C. beticola field populations from Michigan.

scholarly journals Monitoring Fungicide Sensitivity of Cercospora beticola of Sugar Beet for Disease Management Decisions

Plant Disease ◽  
2010 ◽  
Vol 94 (11) ◽  
pp. 1272-1282 ◽  
Author(s):  
Gary A. Secor ◽  
Viviana V. Rivera ◽  
M. F. R. Khan ◽  
Neil C. Gudmestad
Keyword(s):  
United States ◽  
Disease Management ◽  
Sugar Beet ◽  
Leaf Spot ◽  
Fungicide Resistance ◽  
The United States ◽  
Economic Damage ◽  
Cercospora Beticola ◽  
Cercospora Leaf Spot ◽  
Cooperative Effort

Cercospora leaf spot, caused by the fungus Cercospora beticola Sacc., is the most serious and important foliar disease of sugar beet (Beta vulgaris L.) wherever it is grown worldwide. Cercospora leaf spot first caused economic damage in North Dakota and Minnesota in 1980, and the disease is now endemic. This is the largest production area for sugar beet in the United States, producing 5.5 to 6.0 million metric tons on approximately 300,000 ha, which is 56% of the sugar beet production in the United States. This Plant Disease feature article details a cooperative effort among the participants in the sugar beet industry in this growing area and represents a successful collaboration and team effort to confront and change a fungicide resistance crisis to a fungicide success program. As a case study of success for managing fungicide resistance, it will serve as an example to other pathogen–fungicide systems and provide inspiration and ideas for long-term disease management by fungicides.

scholarly journals Rapid Detection of Cercospora beticola in Sugar Beet and Mutations Associated with Fungicide Resistance Using LAMP or Probe-Based qPCR

Plant Disease ◽  
2020 ◽  
Vol 104 (6) ◽  
pp. 1654-1661 ◽  
Author(s):  
Subidhya Shrestha ◽  
Jonathan Neubauer ◽  
Rebecca Spanner ◽  
Mari Natwick ◽  
Joshua Rios ◽  
...  
Keyword(s):  
Sugar Beet ◽  
Fungicide Resistance ◽  
Rapid Detection ◽  
Lamp Assay ◽  
Qpcr Assay ◽  
Cercospora Beticola ◽  
Lamp Method ◽  
In Planta ◽  
Cercospora Leaf Spot

Cercospora leaf spot (CLS), caused by the fungal pathogen Cercospora beticola, is the most destructive disease of sugar beet worldwide. Although growing CLS-tolerant varieties is helpful, disease management currently requires timely application of fungicides. However, overreliance on fungicides has led to the emergence of fungicide resistance in many C. beticola populations, resulting in multiple epidemics in recent years. Therefore, this study focused on developing a fungicide resistance detection “toolbox” for early detection of C. beticola in sugar beet leaves and mutations associated with different fungicides in the pathogen population. A loop-mediated isothermal amplification (LAMP) method was developed for rapid detection of C. beticola in infected sugar beet leaves. The LAMP primers specific to C. beticola (Cb-LAMP) assay was able to detect C. beticola in inoculated sugar beet leaves as early as 1 day postinoculation. A quinone outside inhibitor (QoI)-LAMP assay was also developed to detect the G143A mutation in cytochrome b associated with QoI resistance in C. beticola. The assay detected the mutation in C. beticola both in vitro and in planta with 100% accuracy. We also developed a probe-based quantitative PCR (qPCR) assay for detecting an E198A mutation in β-tubulin associated with benzimidazole resistance and a probe-based qPCR assay for detection of mutations in cytochrome P450-dependent sterol 14α-demethylase (Cyp51) associated with resistance to sterol demethylation inhibitor fungicides. The primers and probes used in the assay were highly efficient and precise in differentiating the corresponding fungicide-resistant mutants from sensitive wild-type isolates.

scholarly journals Genome-wide association studies reveal the complex genetic architecture of DMI fungicide resistance in Cercospora beticola

2020 ◽  
Author(s):  
Rebecca Spanner ◽  
Demetris Taliadoros ◽  
Jonathan Richards ◽  
Viviana Rivera-Varas ◽  
Jonathan Neubauer ◽  
...  
Keyword(s):  
Fungicide Resistance ◽  
Genome Wide Association Study ◽  
Selective Sweep ◽  
Association Studies ◽  
Genome Wide Association ◽  
Cercospora Beticola ◽  
Genome Wide Association Studies ◽  
Synonymous Mutations ◽  
Genome Wide ◽  
A Genome

AbstractCercospora leaf spot is the most important disease of sugar beet worldwide. The disease is caused by the fungus Cercospora beticola and is managed principally by timely application of fungicides including those of the sterol demethylation inhibitor (DMI) class. However, reliance on DMIs has caused an increase in resistance to this class of fungicides in multiple C. beticola populations. To better understand the genetic and evolutionary basis for resistance in C. beticola, a genome-wide association study (GWAS) and selective sweep analysis were conducted for the first time in this fungal plant pathogen. We performed whole genome resequencing of 190 C. beticola isolates predominantly from North Dakota and Minnesota that were phenotyped for sensitivity to tetraconazole, the most widely used DMI fungicide in this region. GWAS identified mutations in genes associated with DMI fungicide resistance including a Regulator of G-protein Signaling (RGS) protein, an ATP-binding cassette (ABC) pleiotropic drug resistance transporter, a dual-specificity tyrosine phosphorylation-regulated kinase (DYRK), and a gene annotated as a hypothetical protein. A SNP upstream of CbCYP51, the gene encoding the target of DMI fungicides, was also identified via GWAS. Haplotype analysis of CbCYP51 identified a synonymous mutation (E170) in high linkage disequilibrium with the upstream SNP, and multiple non-synonymous mutations (L144F, I387M and Y464S) associated with DMI resistance. Additionally, a putative codon bias effect for the L144F substitution was identified that generated different resistance potentials. We also identified a CbCYP51 paralog in C. beticola, CbCYP51-like, with high protein homology to CYP51C found uniquely in Fusarium species but CbCYP51-like does not appear to influence DMI sensitivity. Genome-wide scans of selection showed that several of the GWAS mutations for fungicide resistance resided in regions that have recently undergone a selective sweep. Using radial plate growth on selected media as a fitness proxy, we did not find a trade-off associated with DMI fungicide resistance suggesting that resistance mutations can persist in C. beticola populations. Taken together, we show that population genomic data from a crop pathogen can allow the identification of mutations conferring fungicide resistance and inform about their origins in the pathogen population.

Optimizing management of cercospora leaf spot (Cercospora beticola) of sugarbeet in the wake of fungicide resistance

2019 ◽  
Vol 41 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Sherri L. Tedford ◽  
Rishi R. Burlakoti ◽  
Arthur W. Schaafsma ◽  
Cheryl L. Trueman
Keyword(s):  
Leaf Spot ◽  
Fungicide Resistance ◽  
Cercospora Beticola ◽  
Cercospora Leaf Spot

scholarly journals Genome-Wide Association and Selective Sweep Studies Reveal the Complex Genetic Architecture of DMI Fungicide Resistance in Cercospora beticola

2021 ◽  
Vol 13 (9) ◽  
Author(s):  
Rebecca Spanner ◽  
Demetris Taliadoros ◽  
Jonathan Richards ◽  
Viviana Rivera-Varas ◽  
Jonathan Neubauer ◽  
...  
Keyword(s):  
Fungicide Resistance ◽  
Polyketide Synthase ◽  
Genome Wide Association Study ◽  
Selective Sweep ◽  
Pathogenic Fungus ◽  
Genome Wide Association ◽  
Cercospora Beticola ◽  
Genome Wide ◽  
A Genome ◽  
Dmi Resistance

Abstract The rapid and widespread evolution of fungicide resistance remains a challenge for crop disease management. The demethylation inhibitor (DMI) class of fungicides is a widely used chemistry for managing disease, but there has been a gradual decline in efficacy in many crop pathosystems. Reliance on DMI fungicides has increased resistance in populations of the plant pathogenic fungus Cercospora beticola worldwide. To better understand the genetic and evolutionary basis for DMI resistance in C. beticola, a genome-wide association study (GWAS) and selective sweep analysis were conducted for the first time in this species. We performed whole-genome resequencing of 190 C. beticola isolates infecting sugar beet (Beta vulgaris ssp. vulgaris). All isolates were phenotyped for sensitivity to the DMI tetraconazole. Intragenic markers on chromosomes 1, 4, and 9 were significantly associated with DMI fungicide resistance, including a polyketide synthase gene and the gene encoding the DMI target CbCYP51. Haplotype analysis of CbCYP51 identified a synonymous mutation (E170) and nonsynonymous mutations (L144F, I387M, and Y464S) associated with DMI resistance. Genome-wide scans of selection showed that several of the GWAS mutations for fungicide resistance resided in regions that have recently undergone a selective sweep. Using radial plate growth on selected media as a fitness proxy, we did not find a trade-off associated with DMI fungicide resistance. Taken together, we show that population genomic data from a crop pathogen can allow the identification of mutations conferring fungicide resistance and inform about their origins in the pathogen population.

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