scholarly journals Fitness, Competitive Ability, and Mutation Stability of Isolates of Colletotrichum acutatum from Strawberry Resistant to QoI Fungicides

2018 ◽  
Vol 108 (4) ◽  
pp. 462-468 ◽  
Author(s):  
Bruna B. Forcelini ◽  
Carolina S. Rebello ◽  
Nan-Yi Wang ◽  
Natalia A. Peres
Keyword(s):  
Competitive Ability ◽  
The United States ◽  
Fruit Production ◽  
Field Resistance ◽  
Relative Fitness ◽  
Colletotrichum Acutatum ◽  
Qoi Fungicides ◽  
Quinone Outside Inhibitor ◽  
Production Areas

Quinone-outside inhibitor (QoI) fungicides are used to manage anthracnose of strawberry, caused by Colletotrichum acutatum. However, selection for resistance to QoI fungicides was first reported in 2013 in Florida and, subsequently, in strawberry nurseries and production areas across the United States and Canada. C. acutatum resistance to QoIs is associated with the G143A point mutation in the cytochrome b gene. This mutation is known to be associated with field resistance even at high rates of QoI. In this study, we investigated the relative fitness and competitive ability of QoI-resistant and -sensitive C. acutatum isolates. A fitness comparison did not indicate any difference between resistant and sensitive isolates in aggressiveness, spore production, and mycelial growth at different temperatures. Additionally, in the absence of selection pressure, resistant and sensitive isolates were equally competitive. Cultivation of QoI-resistant and QoI-sensitive isolates for four culture cycles in vitro in the absence of azoxystrobin showed that QoI resistance was stable. The observed lack of fitness penalties and stability of the G143A mutation in QoI-resistant C. acutatum populations suggest that the interruption and further reintroduction of QoI fungicides might not be an option for strawberry nurseries and fruit production areas. Further investigation of alternative chemical and nonchemical C. acutatum control practices, in addition to the integration of multisite fungicides, is needed to reduce the occurrence and distribution of QoI-resistant populations in strawberry fields.

scholarly journals Baseline Sensitivity of Cercospora zeae-maydis to Quinone Outside Inhibitor Fungicides

Plant Disease ◽  
2011 ◽  
Vol 95 (2) ◽  
pp. 189-194 ◽  
Author(s):  
C. A. Bradley ◽  
D. K. Pedersen
Keyword(s):  
United States ◽  
Leaf Spot ◽  
The United States ◽  
Gray Leaf Spot ◽  
Alternative Respiration ◽  
Baseline Sensitivity ◽  
Qoi Fungicides ◽  
Quinone Outside Inhibitor ◽  
Cercospora Zeae Maydis

Cercospora zeae-maydis, the causal agent of gray leaf spot on corn (Zea mays), can cause severe yield loss in the United States. Quinone outside inhibitor (QoI) fungicides are effective tools that can be used to manage gray leaf spot, and their use has increased in corn production in the United States. In total, 61 C. zeae-maydis isolates collected from fields in which QoI fungicides had never been applied were tested in vitro using azoxystrobin-, pyraclostrobin-, or trifloxystrobin-amended medium to determine the effective fungicide concentration at which 50% of the conidial germination was inhibited (EC50). The effect of salicylhydroxamic acid (SHAM) also was evaluated for seven isolates to determine whether C. zeae-maydis is capable of using alternative respiration in azoxystrobin-amended medium. All seven C. zeae-maydis isolates tested had significantly greater (P < 0.02) EC50 values when SHAM was not included in medium amended with azoxystrobin, indicating that C. zeae-maydis has the potential to utilize alternative respiration to overcome QoI fungicide inhibition in vitro. Baseline EC50 values of azoxystrobin ranged from 0.003 to 0.031 μg/ml, with mean and median values of 0.018 and 0.019 μg/ml, respectively. Baseline EC50 values of pyraclostrobin ranged from 0.0003 to 0.0025 μg/ml, with mean and median values of 0.0010 and 0.0010 μg/ml, respectively. Baseline EC50 values of trifloxystrobin ranged from 0.0004 to 0.0034 μg/ml, with mean and median values of 0.0023 and 0.0024 μg/ml, respectively. These baseline sensitivity values will be used in a fungicide resistance monitoring program to determine whether shifts in sensitivity to QoI fungicides are occurring in C. zeae-maydis populations.

scholarly journals Natamycin, a New Biofungicide for Managing Crown Rot of Strawberry Caused by QoI-Resistant Colletotrichum acutatum

Plant Disease ◽  
2018 ◽  
Vol 102 (9) ◽  
pp. 1687-1695 ◽  
Author(s):  
Stacey E. Haack ◽  
Kelly L. Ivors ◽  
Gerald J. Holmes ◽  
Helga Förster ◽  
James E. Adaskaveg
Keyword(s):  
Field Studies ◽  
The United States ◽  
Pathogen Resistance ◽  
Fruit Production ◽  
Crown Rot ◽  
Colletotrichum Acutatum ◽  
Quinone Outside Inhibitor ◽  
Industry Standards ◽  
Important Disease ◽  
Qoi Resistance

Anthracnose crown rot of strawberry, caused by Colletotrichum acutatum, is an important disease affecting California nursery and fruit production. Preplant dip treatments of transplants with fludioxonil-cyprodinil or azoxystrobin are industry standards for managing the disease and have been used extensively. Following reports of reduced efficacy of azoxystrobin in the field, high levels of quinone outside inhibitor (QoI) resistance were detected in California isolates of the pathogen. Resistance was associated with the G143A mutation in the cytochrome b gene, similar to a previous report from Florida, and there were no detected fitness penalties in pathogenicity or virulence. Therefore, several alternative fungicides were investigated in laboratory and field studies. Subsequently, the new biofungicide natamycin was identified. Baseline sensitivities of 74 isolates of C. acutatum to natamycin were determined to be unimodal, with a range from 0.526 to 1.996 μg/ml (mean 0.973 μg/ml). Although this toxicity was considerably lower than that of azoxystrobin (using sensitive isolates), fludioxonil, or cyprodinil, dip treatments of transplants with natamycin (at 500 or 1000 mg/liter) were highly effective. Disease severity and plant mortality in field studies with inoculated transplants were reduced to similarly low levels as treatments containing fludioxonil, whereas azoxystrobin failed in inoculations with QoI-resistant isolates of C. acutatum. Fruit yield was also significantly increased by natamycin as compared with the inoculated control. Differences in disease susceptibility were observed among cultivars evaluated, with Monterey and Portola more susceptible than Fronteras. Natamycin has a unique mode of action that is different from other fungicides registered on strawberry and, based on this research, was registered in the United States as a preplant, biofungicide dip treatment of strawberry transplants for management of anthracnose crown rot.

scholarly journals Prevalence of QoI resistance and mtDNA diversity in the Irish Zymoseptoria tritici population

2019 ◽  
Vol 58 (1) ◽  
pp. 27-33
Author(s):  
S. Kildea ◽  
D.E. Bucar ◽  
F. Hutton ◽  
S. de la Rosa ◽  
T.E. Welch ◽  
...  
Keyword(s):  
Septoria Tritici Blotch ◽  
Septoria Tritici ◽  
Entire Group ◽  
Zymoseptoria Tritici ◽  
Qoi Fungicides ◽  
Quinone Outside Inhibitor ◽  
Strain Collection ◽  
Increased Sensitivity ◽  
Mtdna Diversity

Abstract The emergence and spread of Quinone outside Inhibitor (QoI) fungicide resistance in the Irish Zymoseptoria tritici population in the early 2000s had immediate impacts on the efficacy of the entire group of fungicides for the control of septoria tritici blotch. As a result, a dramatic reduction in the quantities applied to winter wheat occurred in the following seasons. Even in the absence of these fungicides, the frequency of the resistance allele, G143A in the pathogens mtDNA has remained exceptionally high (>97%), and as such, it can be anticipated that continued poor efficacy of current QoI fungicides will be observed. Amongst the isolates with G143A, differences in sensitivity to the QoI pyraclostrobin were observed in vitro. The addition of the alternative oxidase (AOX) inhibitor salicylhydroxamic acid increased sensitivity in these isolates, suggesting some continued impairment of respiration by the QoI fungicides, albeit weak. Interestingly, amongst those tested, the strains from a site with a high frequency of inserts in the MFS1 transporter gene known to enhance QoI efflux did not exhibit this increase in sensitivity. A total of 19 mtDNA haplotypes were detected amongst the 2017 strain collection. Phylogenetic analysis confirmed the suggestion of a common ancestry of all the haplotypes, even though three of the haplotypes contained at least one sensitive strain.

Resistance to Quinone Outside Inhibitor Fungicides Conferred by the G143A Mutation in Cercospora sojina (Causal Agent of Frogeye Leaf Spot) Isolates from Michigan, Minnesota, and Nebraska Soybean Fields

2020 ◽  
Vol 21 (4) ◽  
pp. 230-231 ◽  
Author(s):  
Danilo L. Neves ◽  
Martin I. Chilvers ◽  
Tamra A. Jackson-Ziems ◽  
Dean K. Malvick ◽  
Carl A. Bradley
Keyword(s):  
United States ◽  
Leaf Spot ◽  
Fungicide Resistance ◽  
The United States ◽  
Pcr Assay ◽  
Cercospora Sojina ◽  
Qoi Fungicides ◽  
Quinone Outside Inhibitor ◽  
Frogeye Leaf Spot ◽  
Important Disease

Frogeye leaf spot, caused by Cercospora sojina, is an important disease of soybean (Glycine max) in the United States. An important tactic to manage frogeye leaf spot is to apply foliar fungicides. Isolates of C. sojina were collected from soybean fields in one county in Michigan, three counties in Minnesota, and 10 counties in Nebraska in 2019, and they were tested for resistance to quinone outside inhibitor (QoI) fungicides using a discriminatory dose assay, a PCR assay, and DNA sequencing. Results of the testing indicated that QoI fungicide-resistant isolates were detected in isolates from all counties. Testing results also indicated that the G143A mutation was responsible for the QoI fungicide resistance. This is the first report of QoI fungicide-resistant C. sojina isolates in Michigan, Minnesota, and Nebraska and expands the geographical distribution of QoI fungicide-resistant C. sojina isolates to 18 states in total.

scholarly journals Sensitivity of Bipolaris oryzae Isolates Pathogenic on Cultivated Wild Rice to the Quinone Outside Inhibitor Azoxystrobin

Plant Disease ◽  
2019 ◽  
Vol 103 (8) ◽  
pp. 1910-1917 ◽  
Author(s):  
Claudia V. Castell-Miller ◽  
Deborah A. Samac
Keyword(s):  
Cytochrome B ◽  
Fungicide Resistance ◽  
Wild Rice ◽  
Brown Spot ◽  
Bipolaris Oryzae ◽  
Qoi Fungicides ◽  
Quinone Outside Inhibitor ◽  
Group I ◽  
Mitochondrial Cytochrome B

The occurrence of fungal brown spot, caused by Bipolaris oryzae, has increased in cultivated wild rice (Zizania palustris) paddies in spite of the use of azoxystrobin-based fungicides. The active ingredient blocks electron transfer at the quinone outside inhibitor (QoI) site in the mitochondrial cytochrome b within the bc1 complex, thus obstructing respiration. The in vitro averaged EC50 of baseline isolates collected in 2007 before widespread fungicide use was estimated to be 0.394 µg/ml with PROBIT and 0.427 µg/ml with linear regression analyses. Isolates collected during 2008, 2015, and 2016 had a range of sensitivity as measured by relative spore germination (RG) at a discriminatory dose of 0.4 µg/ml azoxystrobin. Isolates with a higher (≥80%) and lower RG (≤40%) had the wild type nucleotides at amino acid positions F129, G137, and G143 of cytochrome b, sites known to be associated with QoI fungicide resistance. Two Group I introns were found in the QoI target area. The splicing site for the second intron was found immediately after the codon for G143. A mutation for fungicide resistance at this location would hinder splicing and severely reduce fitness. B. oryzae expresses an alternative oxidase in vitro, which allows the fungus to survive inhibition of respiration by azoxystrobin. This research indicates that B. oryzae has not developed resistance to QoI fungicides, although monitoring for changes in sensitivity should be continued. Judicious use of QoI fungicides within an integrated disease management system will promote an effective and environmentally sound control of the pathogen in wild rice paddies.

scholarly journals Effects of SHAM on the Sensitivity of Sclerotinia sclerotiorum and Botrytis cinerea to QoI Fungicides

Plant Disease ◽  
2019 ◽  
Vol 103 (8) ◽  
pp. 1884-1888 ◽  
Author(s):  
Hongjie Liang ◽  
Jinli Li ◽  
Chaoxi Luo ◽  
Jianhong Li ◽  
Fu-Xing Zhu
Keyword(s):  
Botrytis Cinerea ◽  
Sclerotinia Sclerotiorum ◽  
Mycelial Growth ◽  
Control Efficacy ◽  
Vitro Assay ◽  
Qoi Fungicides ◽  
Quinone Outside Inhibitor ◽  
Fungal Phytopathogens ◽  
The Ideal

It is a common practice to add salicylhydroxamic acid (SHAM) into artificial medium in the in vitro sensitivity assay of fungal phytopathogens to the quinone outside inhibitor (QoI) fungicides. The rationale for adding SHAM is to inhibit fungal alternative oxidase, which is presumed to be inhibited by secondary metabolites of plants. Therefore, the ideal characteristics of SHAM should be almost nontoxic to phytopathogens and have no significant effect on control efficacy of fungicides. However, this study showed that the average effective concentration for 50% inhibition (EC50) of mycelial growth values of SHAM were 97.5 and 401.4 μg/ml for Sclerotinia sclerotiorum and Botrytis cinerea, respectively. EC50 values of the three QoI fungicides azoxystrobin, kresoxim-methyl, and trifloxystrobin in the presence of SHAM at 20 and 80 μg/ml for S. sclerotiorum and B. cinerea, respectively, declined by 52.7 to 78.1% compared with those without SHAM. For the dicarboximide fungicide dimethachlone, the average EC50 values in the presence of SHAM declined by 18.2% (P = 0.008) for S. sclerotiorum and 35.9% (P = 0.012) for B. cinerea. Pot experiments showed that SHAM increased control efficacy of the three QoI fungicides against the two pathogens by 43 to 83%. For dimethachlone, SHAM increased control efficacy by 134% for S. sclerotiorum and 86% for B. cinerea. Biochemical studies showed that SHAM significantly inhibited peroxidase activity (P = 0.024) of B. cinerea and esterase activity (P = 0.015) of S. sclerotiorum. The strong inhibitions of SHAM per se on mycelial growth of B. cinerea and S. sclerotiorum and significant influences on the sensitivity of the two pathogens to both the QoI fungicides and dimethachlone as well as inhibitions on peroxidase and esterase indicate that SHAM should not be added in the in vitro assay of sensitivity to the QoI fungicides.

scholarly journals Fitness and Competitive Ability of an Azoxystrobin-Resistant G143A Mutant of Magnaporthe oryzae from Perennial Ryegrass

Plant Disease ◽  
2009 ◽  
Vol 93 (10) ◽  
pp. 1044-1049 ◽  
Author(s):  
B. Ma ◽  
W. Uddin
Keyword(s):  
Perennial Ryegrass ◽  
Magnaporthe Oryzae ◽  
Type Strain ◽  
Competitive Ability ◽  
Wild Type Strain ◽  
The United States ◽  
Gray Leaf Spot ◽  
Relative Fitness ◽  
Wild Type ◽  
Development Of Resistance

Development of azoxystrobin resistance in Magnaporthe oryzae from perennial ryegrass has been reported in certain locations in the United States, and possible development of resistance in additional areas is a major concern in the golf course industry. The study was undertaken to evaluate the relative fitness and competitive ability of a field-collected azoxystrobin-resistant G143A mutant by comparing it with a wild-type strain using detached perennial ryegrass blades. A fitness comparison experiment indicated that the disease severity of the wild-type strain was significantly higher than that of the mutant; however, the mutant produced greater secondary inoculum. When inoculated with three mixed populations of resistant and wild-type strains at different ratios, the production of conidia by the wild-type strain increased and that of the mutant decreased after infection occurred in all three populations tested. In an experiment on the effect of various fungicides on the population initially containing 5% of the mutant, preventive application of azoxystrobin allowed 5% of the mutant to dominate the population after the infection. However, other non-quinone outside inhibitor fungicides and mixtures of azoxystrobin with contact fungicides eliminated the entire mutant. This study demonstrates that the wild-type strain of M. oryzae has a competitive advantage over the mutant within the environment tested. Mixtures and alternations of fungicides with different modes of actions may prevent rapid build-up of resistance in the gray leaf spot pathosystem.

Assessment of quinone outside inhibitor sensitivity and frogeye leaf spot race of Cercospora sojina in Georgia soybean

Plant Disease ◽  
2021 ◽  
Author(s):  
Bennett Harrelson ◽  
Bikash Ghimire ◽  
Robert Kemerait ◽  
Albert Culbreath ◽  
Zenglu Li ◽  
...  
Keyword(s):  
Leaf Spot ◽  
Fungicide Resistance ◽  
Mycelial Growth ◽  
The United States ◽  
In Vitro Assays ◽  
Cercospora Sojina ◽  
Quinone Outside Inhibitor ◽  
Frogeye Leaf Spot ◽  
Differential Cultivars

Frogeye leaf spot (FLS), caused by the fungal pathogen Cercospora sojina K. Hara, is a foliar disease of soybean (Glycine max L. (Merr.)) responsible for yield reductions throughout the major soybean producing regions in the world. In the United States, management of FLS relies heavily on the use of resistant cultivars and in-season fungicide applications, specifically within the class of quinone outside inhibitors (QoIs), which has resulted in the development of fungicide resistance in many states. In 2018 and 2019, 80 isolates of C. sojina were collected from six counties in Georgia and screened for QoI fungicide resistance using molecular and in vitro assays, with resistant isolates being confirmed from three counties. Additionally, 50 isolates, including a “baseline isolate” with no prior fungicide exposure, were used to determine the percent reduction of mycelial growth to two fungicides, azoxystrobin and pyraclostrobin, at six concentrations: 0.0001, 0.001, 0.01, 0.1, 1, and 10 g ml-1. Mycelial growth observed for resistant isolates varied significantly from both the sensitive isolates and the baseline isolate for azoxystrobin concentrations of 10, 1, 0.1, and 0.01 g ml-1 and for pyraclostrobin concentrations of 10, 1, 0.1, 0.01 and 0.001 g ml-1. Moreover, 40 isolates were used to evaluate pathogen race on six soybean differential cultivars by assessing susceptible or resistant reactions. Isolate reactions suggested 12 races of C. sojina present in Georgia, four of which have not been previously described. Species richness indicators (rarefaction and abundance-based coverage estimator - ACE) indicated that within-county C. sojina race numbers were undersampled in the present study, suggesting the potential for the presence of either additional undescribed races or known but unaccounted for races in Georgia. However, no isolates were pathogenic on differential cultivar ‘Davis’, carrying the Rcs3 resistance allele, suggesting the gene is still an effective source of resistance in Georgia.

scholarly journals Reduced Sensitivity to Azoxystrobin of Monilinia fructicola Isolates From Brazilian Stone Fruits is Not Associated With Previously Described Mutations in the Cytochrome b Gene

Plant Disease ◽  
2017 ◽  
Vol 101 (5) ◽  
pp. 766-773 ◽  
Author(s):  
Wagner V. Pereira ◽  
Isabela V. Primiano ◽  
Rafael G. F. Morales ◽  
Natalia A. Peres ◽  
Lilian Amorim ◽  
...  
Keyword(s):  
Cytochrome B ◽  
Ex Vivo ◽  
Brown Rot ◽  
Monilinia Fructicola ◽  
Cyt B ◽  
Qoi Fungicides ◽  
Quinone Outside Inhibitor ◽  
Low Sensitivity ◽  
Cyt B Gene

Quinone-outside inhibitor (QoI) fungicides are effective tools for preharvest control of brown rot of stone fruit. These fungicides have a very specific site of action so the risk of resistance selection is high. The sensitivity of Monilinia fructicola (G. Winter) Honey isolates to azoxystrobin (QoI) was investigated in 143 isolates collected between 2002 and 2011 from four Brazilian states in orchards with different frequencies of fungicide use (0 to 6 fungicides sprays/season). Sensitivity of the isolates to azoxystrobin was determined in vitro, by inhibition of mycelial growth and spore germination on fungicide-amended media or ex vivo by pathogen inoculation in untreated or treated fruit with azoxystrobin. Potential mutations in codons 143, 137, and 129 of the cytochrome b (Cyt b) gene and the occurrence of an intron immediately after codon 143 were analyzed in a subpopulation of the isolates. The M. fructicola population of São Paulo State was less sensitive to the fungicide than the population from the states of Paraná, Santa Catarina, and Rio Grande do Sul. The low sensitivity of the isolates was confirmed also by comparing to the sensitivity of the baseline isolates. Mutations in G143A, F129L, and G137R in Cyt b gene were not found. In addition, 58 isolates tested showed an intron after codon 143 in Cyt b gene. Our results indicate that other mechanisms of selection for low sensitivity to QoI fungicides should be investigated.

scholarly journals First Report of the Soybean Frogeye Leaf Spot Fungus (Cercospora sojina) Resistant to Quinone Outside Inhibitor Fungicides in North America

Plant Disease ◽  
2012 ◽  
Vol 96 (5) ◽  
pp. 767-767 ◽  
Author(s):  
G. R. Zhang ◽  
M. A. Newman ◽  
C. A. Bradley
Keyword(s):  
Leaf Spot ◽  
Management Practices ◽  
The United States ◽  
Conidial Germination ◽  
Cercospora Sojina ◽  
Soybean Field ◽  
Qoi Fungicides ◽  
First Report ◽  
Quinone Outside Inhibitor ◽  
Frogeye Leaf Spot

Quinone outside inhibitor (QoI; also known as strobilurin) fungicides sometimes are applied to soybean (Glycine max) fields to help manage frogeye leaf spot of soybean (caused by Cercospora sojina) in the United States. In August 2010, soybean leaflets exhibiting severe frogeye leaf spot symptoms were collected from a field in Lauderdale County, TN that had been treated twice with pyraclostrobin during that growing season. The field had been planted into soybean annually since at least 2008, and a QoI fungicide had been applied to the field in each of those years. Fifteen single-spore isolates of C. sojina were recovered from the affected soybean leaflets. These isolates were identified as C. sojina based on the observed symptoms on the soybean leaflets and the morphology and size of conidiophores and conidia (3). In addition, DNA was extracted from the cultures, PCR amplification of the small subunit rDNA and internal transcribed spacer (ITS) region was conducted (2), and the resulting PCR product was sequenced at the Keck Biotechnology Center at the University of Illinois, Urbana. The resulting nucleotide sequences were compared with sequences deposited in the nucleotide database ( http://www.ncbi.nlm.nih.gov ) and showed highest homology to sequences of C. sojina. The isolates were tested for their sensitivity to technical-grade formulations of the QoI fungicides azoxystrobin, pyraclostrobin, and trifloxystrobin with an in vitro conidial germination assay with fungicide + salicylhydroxamic acid (SHAM)-amended potato dextrose agar as described by Bradley and Pedersen (1). The effective concentration at which 50% conidial germination was inhibited (EC50) was determined for all 15 C. sojina isolates, with mean values of 3.1644 (2.7826 to 4.5409), 0.3297 (0.2818 to 0.6404), and 0.8573 (0.3665 to 2.5119) μg/ml for azoxystrobin, pyraclostrobin, and trifloxystrobin, respectively. When compared with previously established mean EC50 values of C. sojina baseline isolates (4), EC50 values of the C. sojina isolates collected from the Lauderdale County, TN soybean field were approximately 249- to 7,144-fold greater than the EC50 values of the baseline isolates. These results indicate that all isolates recovered from the Lauderdale County, TN soybean field were highly resistant to QoI fungicides. To our knowledge, this is the first report of QoI fungicide resistance occurring in C. sojina, and surveys for additional QoI fungicide-resistant C. sojina isolates are needed to determine their prevalence and geographic distribution. In light of these findings, soybean growers in Tennessee and adjacent states should consider utilizing alternative frogeye leaf spot management practices such as planting resistant cultivars, rotating to nonhost crops, and tilling affected soybean residue (3). References: (1) C. A. Bradley and D. K. Pedersen. Plant Dis. 95:189, 2011. (2) N. S. Lord et al. FEMS Microbiol. Ecol. 42:327, 2002. (3) D. V. Phillips. Page 20 in: Compendium of Soybean Diseases. 4th ed. G. L. Hartman et al., eds. The American Phytopathological Society, St. Paul, MN, 1999. (4) G. Zhang et al. Phytopathology (Abstr.) 100(suppl.):S145, 2010.

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