scholarly journals Characterizing Fenbuconazole and Propiconazole Sensitivity and Prevalence of ‘Mona’ in Isolates of Monilinia fructicola from New York

Plant Disease ◽  
2011 ◽  
Vol 95 (7) ◽  
pp. 828-834 ◽  
Author(s):  
Sara M. Villani ◽  
Kerik D. Cox

Demethylation inhibitor (DMI) resistant populations of Monilinia fructicola, the causal agent of brown rot of stone fruit, and the presence of the genetic DMI resistance determinant ‘Mona’ have been reported throughout the eastern United States. In this study, we endeavored to conduct a comprehensive investigation of DMI sensitivity, the prevalence of ‘Mona’, and implications of DMI use for M. fructicola populations from New York and Pennsylvania. Of the 18 orchards surveyed, only 9 were primarily composed of isolates with either resistance or reduced sensitivity to fenbuconazole and propiconazole. The DMI resistance determinant ‘Mona’ was only found in 5 orchards, present in isolates with a range of sensitivity phenotypes, and not always present in resistant isolates. These results suggested that ‘Mona’ only contributes to a portion of the quantitative resistance response to DMI fungicides. On detached blossoms and fruit, protective applications of fenbuconazole (Indar 2F) against isolates with resistance or reduced sensitivity resulted in significantly (P < 0.05) lower brown rot incidence compared to applications of propiconazole (Orbit 3.6EC) and water controls. By comparison, therapeutic applications of fenbuconazole and propiconazole against isolates with resistance or reduced sensitivity provided little to no reduction in brown rot incidence on blossoms and fruit.

Plant Disease ◽  
2020 ◽  
Author(s):  
Kim Lesniak ◽  
Jingyu Peng ◽  
Tyre J Proffer ◽  
Cory Outwater ◽  
Lauren Eldred ◽  
...  

Resistance to sterol demethylation inhibitor fungicides (DMIs) in Monilinia fructicola, causal agent of brown rot of stone fruit, has been reported in the southeastern and eastern United States and in Brazil. DMI resistance of some M. fructicola isolates, in particular those recovered from the southeastern U.S., is associated with a sequence element termed ‘Mona’ that causes overexpression of the cytochrome demethylase target gene MfCYP51. In this study, we conducted statewide surveys of Michigan stone fruit orchards from 2009-2011 and in 2019, and determined the sensitivity to propiconazole of a total of 813 isolates of M. fructicola. A total of 80.7% of Michigan isolates were characterized as resistant to propiconazole by relative growth assays but the ‘Mona’ insert was not uniformly detected, and was present in some isolates that were not characterized as DMI resistant. Gene expression assays indicated that elevated expression of MfCYP51 was only weakly correlated with DMI-resistance in M. fructicola isolates from Michigan, and there was no obvious correlation between the presence of the ‘Mona’ element and elevated expression of MfCYP51. However, sequence analysis of MfCYP51 from 25 DMI-resistant isolates did not reveal any point mutations that could be correlated with resistance. Amplification and sequencing upstream of MfCYP51 resulted in detection of DNA insertions in a wide range of isolates typed by DMI phenotype and the presence of ‘Mona’ or other unique sequences. The function of these unique sequences or their presence upstream of MfCYP51 cannot be correlated to a DMI-resistant genotype at this time. Our results indicate that DMI resistance was established in Michigan populations of M. fructicola by 2009 to 2011, and that relative resistance levels have continued to increase to the point that practical resistance is present in most orchards. In addition, the presence of the ‘Mona’ insert is not a marker for identifying DMI-resistant isolates of M. fructicola in Michigan.


Plant Disease ◽  
1999 ◽  
Vol 83 (10) ◽  
pp. 913-916 ◽  
Author(s):  
Eldon I. Zehr ◽  
Lynn A. Luszcz ◽  
William C. Olien ◽  
W. C. Newall ◽  
Joe E. Toler

The baseline sensitivity of Monilinia fructicola in a peach orchard not previously exposed to demethylation-inhibiting (DMI) fungicides was determined for propiconazole, using the concentration in an agar medium required to suppress radial growth of mycelium by 50% (EC50) The baseline sensitivity was found to be approximately 0.03 μg/ml. Prolonged, regular exposure of the natural population of M. fructicola to propiconazole in the test orchard over a 3-year period (29 total applications) resulted in a wider range of sensitivity (EC50 of 0.02 to 2.16μg/ml) among isolates than was observed in the initial population (EC50 of 0.02 to 0.15 μg/ml). Comparisons with isolates from commercial orchards where DMI fungicides were used regularly showed that sensitivities were comparable to, or less than, those of isolates from the population in the test orchard that had been exposed to propiconazole for the 3-year period. M. fructicola in South Carolina peach orchards might now be less sensitive to DMI fungicides than when those fungicides were first introduced for brown rot control, although effective disease control in the field has been maintained.


Plant Disease ◽  
2013 ◽  
Vol 97 (8) ◽  
pp. 1063-1068 ◽  
Author(s):  
F. Chen ◽  
X. Liu ◽  
G. Schnabel

In 2012, significant brown rot disease was observed on stone fruit in Pennsylvania, Maryland, and South Carolina despite preharvest application of methyl benzimidazole carbamate (MBC) and demethylase inhibitor (DMI) fungicides. In total, 140 Monilinia fructicola isolates were collected from diseased orchards and examined for fungicide sensitivity. In addition to isolates resistant to either the DMI propiconazole or the MBC thiophanate-methyl, 22 isolates were discovered that were resistant to both fungicides, including 4 isolates from peach in South Carolina, 12 isolates from peach and sweet cherry in Maryland, and 6 isolates from sweet cherry in Pennsylvania. Analysis of MBC resistance revealed that dual-resistant isolates from South Carolina carried the β-tubulin E198A mutation, whereas isolates from Maryland and Pennsylvania carried E198 mutations not previously described in the Monilinia genus, E198Q or F200Y. The genetic element Mona, associated with DMI fungicide resistance in M. fructicola, was detected in the dual-resistant isolates from South Carolina but not in the isolates from the two more northern states. An investigation into the molecular mechanism of DMI resistance in the latter isolates revealed that resistance was not based on increased expression or mutation of MfCYP51, which encodes the target of DMI fungicides. Label rates of formulated propiconazole or thiophanate-methyl were unable to control dual-resistant isolates on detached peach fruit, confirming field relevance of dual resistance. The same isolates were not affected by fitness penalties based on mycelial growth rate, ability to sporulate, and virulence on detached peach fruit. The emergence of M. fructicola strains resistant to both DMI and MBC fungicides in multiple states and multiple stone fruit crops is a significant development and needs to be considered when designing resistance management strategies in stone fruit orchards.


Plant Disease ◽  
2012 ◽  
Vol 96 (3) ◽  
pp. 416-422 ◽  
Author(s):  
F. P. Chen ◽  
J. R. Fan ◽  
T. Zhou ◽  
X. L. Liu ◽  
J. L. Liu ◽  
...  

Sterol 14α-demethylase inhibitors (DMIs) continue to be important in the management of brown rot of Monilinia spp. worldwide. In this study, the sensitivity of 100 Monilinia fructicola isolates from four unsprayed orchards and two packinghouses in Beijing, China, to the new DMI fungicide SYP-Z048 was evaluated and ranged from 0.003 to 0.039 and 0.016 to 0.047 μg/ml, respectively. Laboratory mutants resistant to SYP-Z048 were generated using UV irradiation but no mutants occurred spontaneously. Resistance was stable after 10 weekly consecutive transfers on fungicide-free medium. Three parameters, including growth rate, sporulation in vitro, and lesion area, were significantly different when sensitive isolates and resistant mutants were analyzed as groups. Mutants grew more slowly and developed significantly smaller lesions on detached fruit, and their sporulation ability in vitro was reduced. Cross resistance was found between SYP-Z048 and propiconazole (ρ = 0.82, P < 0.0001) but not between SYPZ048 and tridemorph, carbendazim, procymidone, azoxystrobin, or pyrimethanil. SYP-Z048 resistance in mutants exhibiting 50% mycelial growth inhibition values greater than 0.3 μg/ml was correlated with the presence of a mutation in the CYP51 gene that encodes the target protein for DMI fungicides. The mutation caused an amino acid change from tyrosine to phenylalanine at position 136 (Y136F). To our knowledge, this is the first baseline sensitivity of M. fructicola collected from China to a DMI fungicide. The inability of M. fructicola to generate spontaneous DMI-resistant mutants coupled with reduced fitness of Y136F mutants can explain why this target site mutation has not yet emerged as a DMI fungicide resistance determinant in M. fructicola field populations worldwide.


Plant Disease ◽  
2004 ◽  
Vol 88 (9) ◽  
pp. 1000-1004 ◽  
Author(s):  
Guido Schnabel ◽  
P. Karen Bryson ◽  
William C. Bridges ◽  
Phillip M. Brannen

Single-spore isolates of Monilinia fructicola were collected from commercial orchards in South Carolina and Georgia with prolonged past exposure to demethylation inhibitor (DMI) fungicides and from an orchard with no DMI history (baseline population). Sensitivity to propiconazole was determined using the concentration in agar media required to suppress radial growth of mycelium by 50% (EC50. Mean EC50 values from six South Carolina populations were not different from the baseline population (P < 0.05). Two of five populations from Georgia revealed (significantly higher mean EC50 values compared with the baseline population (P < 0.05). Isolates with high (AP5 and AP6) and low (DL71 and DL72) EC50 values were selected to determine disease incidence on peach fruit after protective or curative applications of propiconazole at 0.15 or 0.3 liter/ha (half and full label rate, respectively). Disease incidence was significantly greater on peaches inoculated with AP5 and AP6 after curative treatment with propiconazole at 0.15 liter/ha (P < 0.05). Following protective or curative treatments at 0.3 liter/ha, disease incidence was significantly greater for AP6 but not for AP5. These results suggest that a shift toward reduced sensitivity has developed in some M. fructicola populations from Georgia, and that isolates with reduced sensitivity to propiconazole are more difficult to control in the field. Field testing of DMI fungicides, captan, QoI fungicides, and fenhexamid in experimental orchards) indicated that the DMI fungicides are still among the most efficacious products for brown rot (control, and that new products containing QoI fungicides may be viable disease control alternatives or rotation partners.


Plant Disease ◽  
2008 ◽  
Vol 92 (7) ◽  
pp. 1099-1103 ◽  
Author(s):  
Chao-Xi Luo ◽  
Kerik D. Cox ◽  
Achour Amiri ◽  
Guido Schnabel

Sterol demethylation inhibitor (DMI) fungicide resistance in isolates of Monilinia fructicola from Georgia has been linked to overexpression of the MfCYP51 gene and a corresponding 65-bp genetic element ‘Mona’ inserted in the upstream region of MfCYP51. In this study, a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was developed to detect the Mona element. Fourteen DMI fungicide-resistant (DMI-R) and six DMI fungicide-sensitive (DMI-S) isolates from Georgia, six DMI-R and 11 DMI-S isolates from South Carolina, seven DMI-R and nine DMI-S isolates from New York, and two DMI-R and three DMI-S isolates from Ohio were used in this study. The isolates from the southeastern United States and Ohio were collected from peach, whereas isolates from New York were collected from cherry. A 376-bp fragment containing the Mona element was consistently amplified with primer pair INS65-F and INS65-R from DMI-R isolates, and either a 311-bp or 1,815-bp fragment was amplified from DMI-S isolates. The primer pair did not amplify DNA fragments of similar sizes from isolates of five other common fruit rot pathogens of peach, including Alternaria alternata, Colletotrichum acutatum, Gilbertella persicaria, Penicillium expansum, and Rhizopus stolonifer. Gel electrophoresis of the PCR amplicon can distinguish between DMI-R and DMI-S isolates based on the 65-bp size difference of the amplicon; however, the restriction digestion assay can verify questionable results, especially in the absence of a positive control. Only the 376-bp fragment containing the Mona element was digestable with endonuclease BsrBI, resulting in two restriction fragments of 236 and 140 bp in size. In this study, a protocol for Mona detection from aerial fungal structures was developed that can yield results within a few hours of sampling. This study confirms that the Mona element is strongly linked to the DMI-resistance phenotype and reveals that overexpression of the MfCYP51 gene is a common DMI fungicide resistance mechanism in M. fructicola, not only in Georgia but throughout the eastern United States.


1999 ◽  
Vol 64 (4) ◽  
pp. 653-658 ◽  
Author(s):  
John P. Hart ◽  
C. Margaret Scarry

AbstractA radiocarbon date of A.D. 1070 ± 60 was linked to the remains of maize (Zea mays), beans (Phaseolus vulgaris), and squash (Cucñrbita pepo) at the Roundtop site in the Susquehanna River valley of New York by William Ritchie in 1969 and 1973 publications. This date established the presence of beans in the Northeast at an earlier time than in most other areas of the eastern United States, where they are generally rare before A.D. 1300. Subsequently beans have been reported in pre-A.D.1300 contexts from at least eight other sites in the Northeast. Recent calibrated AMS dates on beans from Roundtop are no earlier than A.D. 1300 (Hart 1999a). Given that the original Roundtop date was responsible for the acceptance of early beans in the Northeast, the AMS dates suggested that beans may not become archaeologically visible there until ca. A.D. 1300. AMS dates on beans from four other sites, reported here, substantiate the Roundtop results. Beans and by extension maize-beans-squash intercropping are not evident in the Northeast before ca. A.D. 1300.


Plant Disease ◽  
2009 ◽  
Vol 93 (4) ◽  
pp. 386-394 ◽  
Author(s):  
George W. Sundin ◽  
Nicole A. Werner ◽  
Keith S. Yoder ◽  
Herb S. Aldwinckle

The bacterial antagonists Pseudomonas fluorescens A506, Pantoea agglomerans C9-1, and Pantoea agglomerans E325 and preparations of Bacillus subtilis QST 713 containing bacterial endospores and lipopeptide metabolites were evaluated for efficacy in controlling fire blight in Michigan, New York, and Virginia. When examined individually, the biological control materials were not consistently effective in reducing blossom infection. The average reduction in blossom infection observed in experiments conducted between 2001 and 2007 was variable and ranged from 9.1 to 36.1%, while control with streptomycin was consistent and ranged from 59.0 to 67.3%. Incidence of blossom colonization by the bacterial antagonists was inconsistent, and <60% of stigmata had the antagonists present in 12 of 25 experiments. Consistent control of blossom infection was observed when the biological control materials were integrated into programs with streptomycin, resulting in a reduction of the number of streptomycin applications needed to yield similar levels of control. Our results indicate that the prospects for biological control of fire blight in the eastern United States are currently not high due to the variability in efficacy of existing biological control options.


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