Field Strains of Monilinia fructicola Resistant to Both MBC and DMI Fungicides Isolated from Stone Fruit Orchards in the Eastern United States

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.

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Reduced Sensitivity in Monilinia fructicola to Propiconazole in Georgia and Implications for Disease Management

Plant Disease ◽

10.1094/pdis.2004.88.9.1000 ◽

2004 ◽

Vol 88 (9) ◽

pp. 1000-1004 ◽

Cited By ~ 59

Author(s):

Guido Schnabel ◽

P. Karen Bryson ◽

William C. Bridges ◽

Phillip M. Brannen

Keyword(s):

South Carolina ◽

Disease Incidence ◽

Brown Rot ◽

Field Testing ◽

Monilinia Fructicola ◽

Single Spore ◽

Peach Fruit ◽

Dmi Fungicides ◽

Agar Media ◽

Population Sensitivity

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.

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First report of Anthracnose on Peach Fruit Caused by Colletotrichum siamense in Uruguay

Plant Disease ◽

10.1094/pdis-05-21-0950-pdn ◽

2021 ◽

Author(s):

María Julia Carbone ◽

Victoria Moreira ◽

Pedro Mondino ◽

Sandra Alaniz

Keyword(s):

South Carolina ◽

Prunus Persica ◽

Disease Incidence ◽

Management Strategies ◽

Control Treatment ◽

Fluorescent Light ◽

Peach Fruit ◽

First Report ◽

Anthracnose Disease ◽

Equidistant Points

Peach (Prunus persica L.) is an economically important deciduous fruit crop in Uruguay. Anthracnose caused by species of the genus Colletotrichum is one of the major diseases in peach production, originating significant yield losses in United States (Hu et al. 2015), China (Du et al. 2017), Korea (Lee et al. 2018) and Brazil (Moreira et al. 2020). In February 2017, mature peach fruits cv. Pavia Canario with symptoms resembling anthracnose disease were collected from a commercial orchard located in Rincon del Colorado, Canelones, in the Southern region of Uruguay. Symptoms on peach fruit surface were characterized as circular, sunken, brown to dark-brown lesions ranging from 1 to 5 cm in diameter. Lesions were firm to touch with wrinkled concentric rings. All lesions progressed to the fruit core in a V-shaped pattern. The centers of the lesions were covered by orange conidial masses. Monosporic isolates obtained from the advancing margin of anthracnose lesions were grown on PDA at 25ºC and 12h photoperiod under fluorescent light. The representative isolates DzC1, DzC2 and DzC6 were morphologically and molecularly characterized. Upper surface of colonies varied from white or pale-gray to gray and on the reverse dark-gray with white to pale-gray margins. Conidia were cylindrical, with both ends predominantly rounded or one slightly acute, hyaline and aseptate. The length and width of conidia ranged from 9.5 to 18.9 µm (x ̅=14.1) and from 3.8 to 5.8 µm (x ̅=4.6), respectively. The ACT, βTUB2, GAPDH, APN2, APN2/MAT-IGS, and GAP2-IGS gene regions were amplified and sequenced with primers ACT-512F/ACT-783R (Carbone and Kohn, 1999), BT2Fd/BT4R (Woudenberg et al. 2009), GDF1/GDR1 (Guerber et al. 2003), CgDLR1/ColDLF3, CgDLF6/CgMAT1F2 (Rojas et al. 2010) and GAP1041/GAP-IGS2044 (Vieira et al. 2017) respectively and deposited in the GenBank database (MZ097888 to MZ097905). Multilocus phylogenetic analysis revealed that Uruguayan isolates clustered in a separate and well supported clade with sequences of the ex-type (isolate ICMP 18578) and other C. siamense strains (isolates Coll6, 1092, LF139 and CMM 4248). To confirm pathogenicity, mature and apparently healthy peach fruit cv. Pavia Canario were inoculated with the three representative isolates of C. siamense (six fruit per isolate). Fruit were surface disinfested with 70% ethanol and wounded with a sterile needle at two equidistant points (1 mm diameter x 1 mm deep). Then, fruit were inoculated with 5 µl of a spore suspension (1×106 conidia mL-1) in four inoculation points per fruit (two wounded and two unwounded). Six fruit mock-inoculated with 5 µl sterile water were used as controls. Inoculated fruit were placed in moist chamber and incubated at 25°C during 10 days. Anthracnose lesions appeared at 2 and 4 days after inoculation in wounded and unwounded points, respectively. After 7 days, disease incidence was 100% and 67% for wounded and unwounded fruit, respectively. The control treatment remained symptomless. The pathogens were re-isolated from all lesions and re-identified as C. siamense. C. siamense was previously reported in South Carolina causing anthracnose on peach (Hu et al. 2015). To our knowledge, this is the first report of anthracnose disease on peach caused by C. siamense in Uruguay. Effective management strategies should be implemented to control anthracnose and prevent the spread of this disease to other commercial peach orchards.

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Identification and Characterization of Benzimidazole Resistance in Monilinia fructicola from Stone Fruit Orchards in California

Applied and Environmental Microbiology ◽

10.1128/aem.69.12.7145-7152.2003 ◽

2003 ◽

Vol 69 (12) ◽

pp. 7145-7152 ◽

Cited By ~ 127

Author(s):

Zhonghua Ma ◽

Michael A. Yoshimura ◽

Themis J. Michailides

Keyword(s):

Dna Sequences ◽

Point Mutations ◽

Brown Rot ◽

Stone Fruit ◽

Monilinia Fructicola ◽

Tubulin Gene ◽

Benzimidazole Fungicides ◽

Specific Pcr ◽

Allele Specific ◽

Fruit Orchards

ABSTRACT Low and high levels of resistance to the benzimidazole fungicides benomyl and thiophanate-methyl were observed in field isolates of Monilinia fructicola, which is the causative agent of brown rot of stone fruit. Isolates that had low levels of resistance (hereafter referred to as LR isolates) and high levels of resistance (hereafter referred to as HR isolates) were also cold and heat sensitive, respectively. Results from microsatellite DNA fingerprints showed that genetic identities among the populations of sensitive (S), LR, and HR isolates were very high (>0.96). Analysis of DNA sequences of theβ -tubulin gene showed that the LR isolates had a point mutation at codon 6, causing a replacement of the amino acid histidine by tyrosine. Codon 198, which encodes a glutamic acid in S and LR isolates, was converted to a codon for alanine in HR isolates. Based on these point mutations in the β-tubulin gene, allele-specific PCR assays were developed for rapid detection of benzimidazole-resistant isolates of M. fructicola from stone fruit.

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Discontinuance of tebuconazole in the field restores sensitivity of Monilinia fructicola in stone fruit orchards

Plant Pathology ◽

10.1111/ppa.13101 ◽

2019 ◽

Vol 69 (1) ◽

pp. 68-76 ◽

Cited By ~ 4

Author(s):

W. V. Pereira ◽

R. G. F. Morales ◽

A. I. G. Bauer ◽

K. Kudlawiec ◽

L. L. May‐De‐Mio

Keyword(s):

Stone Fruit ◽

Monilinia Fructicola ◽

Fruit Orchards

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Sensitivity of Monilinia fructicola from Stone Fruit to Thiophanate-Methyl, Iprodione, and Tebuconazole

Plant Disease ◽

10.1094/pdis.2004.88.4.373 ◽

2004 ◽

Vol 88 (4) ◽

pp. 373-378 ◽

Cited By ~ 39

Author(s):

Michael A. Yoshimura ◽

Yong Luo ◽

Zhonghua Ma ◽

Themis J. Michailides

Keyword(s):

Mycelial Growth ◽

Effective Concentration ◽

Stone Fruit ◽

Monilinia Fructicola ◽

Thiophanate Methyl ◽

Current Population ◽

Full Dosage

Sensitivity in Monilinia fructicola to three fungicides was determined by measuring mycelial growth in fungicide-amended media. Resistance to thiophanate-methyl was found in 39 of 52 isolates (75%) collected from 1992 to 1998 (historic population) and 22 of 100 isolates (22%) collected in 2002 (current population). Three groups having distinct ranges of values for 50% effective concentration (EC50) to thiophanate-methyl were identified. Benzimidazole-sensitive (benS) isolates had EC50 values less than 2.0, low-resistant (benL) isolates between 2.0 and 30.0, and high-resistant (benH) isolates greater than 30.0 μg/ml. One (2%) isolate from the historic and three (3%) isolates from the current population were benH. Inoculation of untreated nectarine blossoms with four isolates from each of the three groups, individually or combined using equal numbers of conidia from each isolate, showed that the benS, benL, and benH isolates were equally pathogenic and competitive. Use of thiophanate-methyl at 300 μg a.i./ml (half dosage) and 600 μg a.i./ml (full dosage) effectively reduced the percentage of blighted blossoms caused by the benS group but not that caused by the benL and benH groups. The benH isolates caused significantly greater percentage of blighted blossoms than the benL isolates at both dosage levels. None of the tested isolates of M. fructicola were resistant to either iprodione or tebuconazole.

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Resistance in Colletotrichum siamense From Peach and Blueberry to Thiophanate-Methyl and Azoxystrobin

Plant Disease ◽

10.1094/pdis-10-14-1077-re ◽

2015 ◽

Vol 99 (6) ◽

pp. 806-814 ◽

Cited By ~ 34

Author(s):

Meng-Jun Hu ◽

Anja Grabke ◽

Madeline E. Dowling ◽

Helen J. Holstein ◽

Guido Schnabel

Keyword(s):

South Carolina ◽

Field Resistance ◽

Fruit Rot ◽

Nucleotide Sequence Analysis ◽

Cytb Gene ◽

Single Spore ◽

Peach Fruit ◽

Thiophanate Methyl ◽

Colletotrichum Siamense ◽

Commercial Operation

Anthracnose fruit rot was observed in some late-season peach cultivars in South Carolina in the 2012 and 2013 production seasons as well as increased anthracnose leaf spot of blueberry in a commercial operation of the same state in 2012. Single-spore isolates of Colletotrichum siamense were either sensitive or resistant to both thiophanate-methyl and azoxystrobin with the concentration of the fungicide at which fungal development is inhibited by 50% of ≥100 μg/ml. Resistant isolates revealed the E198A mutation in β-tubulin and the G143A mutation in cytochrome b. Nucleotide sequence analysis of the complete CYTB gene from genomic DNA of C. siamense isolates revealed an intronless genotype (CsI) and a genotype revealing two introns (CsII) at amino acid positions 131 and 164. Resistance to thiophanate-methyl or azoxystrobin was not found in isolates of C. fructicola collected from peach fruit. The CYTB gene of isolates of this species was of the CfII genotype or revealed a unique CfIIa genotype. Phylogenetic analysis of C. siamense isolates from different locations and different crops showed that the resistant isolates were genetically closer to each other than to sensitive isolates, suggesting that field resistance to thiophanate-methyl and azoxystrobin fungicides is derived from a common ancestor.

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

Plant Disease ◽

10.1094/pdis-12-10-0943 ◽

2011 ◽

Vol 95 (7) ◽

pp. 828-834 ◽

Cited By ~ 16

Author(s):

Sara M. Villani ◽

Kerik D. Cox

Keyword(s):

New York ◽

No Reduction ◽

Quantitative Resistance ◽

Brown Rot ◽

Resistance Determinant ◽

Monilinia Fructicola ◽

Eastern United States ◽

Resistance Response ◽

Dmi Fungicides ◽

Dmi Resistance

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.

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A New Selective Medium for the Recovery and Enumeration of Monilinia fructicola, M. fructigena, and M. laxa from Stone Fruits

Phytopathology ◽

10.1094/phyto-99-10-1199 ◽

2009 ◽

Vol 99 (10) ◽

pp. 1199-1208 ◽

Cited By ~ 4

Author(s):

Achour Amiri ◽

Imre J. Holb ◽

Guido Schnabel

Keyword(s):

South Carolina ◽

Mycelial Growth ◽

Selective Medium ◽

Ammonium Molybdate ◽

Potato Dextrose Agar ◽

Penicillium Expansum ◽

Colletotrichum Acutatum ◽

Monilinia Fructicola ◽

Stone Fruits ◽

Peach Fruit

Isolation of Monilinia spp. from stone and pome fruit surfaces is difficult due to the presence of several fast-growing fungal species such as Rhizopus, Alternaria, and Penicillium spp. Therefore, a new selective medium (acidified potato dextrose agar [pH 3.6] amended with fosetyl-aluminum [fosetyl-AL] at 500 μg/ml) (APDA-F500) was developed for the recovery of Monilinia propagules. The antifungal agents fosetyl-Al, dichloran, ammonium molybdate, and 2-deoxy-D-glucose (2-dD-glucose) were tested in potato dextrose agar (PDA) for their selective activity against Monilinia fructicola and seven common fungal contaminants of peach, including Alternaria alternata, Aspergillus niger, Colletotrichum acutatum, Gilbertella persicaria, Penicillium expansum, Phomopsis amygdali, and Rhizopus stolonifer. Dichloran, ammonium molybdate, and 2-dD-glucose inhibited spore germination and mycelial growth of all test fungi, including M. fructicola, at comparable levels. Fosetyl-Al added to PDA (PDA-F) at 500 or 1,000 μg/ml did not inhibit germination of any of the fungi but had a strong effect on mycelial growth of six of eight test fungi at 1,000 μg/ml, with the exceptions being R. stolonifer and M. fructicola. Germination and mycelial growth of M. fructicola were least affected on APDA-F500 compared with the other test fungi. On APDA-F500 at pH 3.2 and 3.6, germination of M. fructicola was not inhibited but mycelial growth was reduced by 54.2 and 24.2%, respectively. In all, 17 M. fructicola, 6 M. fructigena, and 6 M. laxa isolates collected from different geographic locations and diverse hosts were evaluated for their germination and mycelial growth on APDA-F500 (at pH 3.6). Germination was not inhibited for any isolate and relative mycelial growth was 45.8 to 83.3%. Field-grown peach fruit from South Carolina and Hungary and plum fruit from Hungary were used to test the selectivity of APDA-F500 for the recovery of three Monilinia spp. compared with PDA-F500 and Monilinia selective medium (MSM) previously developed for Monilinia spp. detection. Percent recovery of M. fructicola from South Carolinian peach fruit was highest on APDA-F500 (0, 17, and 69% in June, July, and August, respectively) compared with PDA-F500 (0, 3.5, and 50%, respectively) and MSM (0, 0, and 6.8%, respectively). Moreover, APDA-F500 selectively recovered M. fructigena and M. laxa propagules from the surfaces of Hungarian peach and plum fruit. Our results indicate that APDA-F500 is a useful medium for selective isolation and enumeration of the three most common Monilinia spp. attacking stone fruits worldwide.

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Reduced Sensitivity in Monilinia fructicola to Propiconazole Following Prolonged Exposure in Peach Orchards

Plant Disease ◽

10.1094/pdis.1999.83.10.913 ◽

1999 ◽

Vol 83 (10) ◽

pp. 913-916 ◽

Cited By ~ 54

Author(s):

Eldon I. Zehr ◽

Lynn A. Luszcz ◽

William C. Olien ◽

W. C. Newall ◽

Joe E. Toler

Keyword(s):

South Carolina ◽

Radial Growth ◽

Prolonged Exposure ◽

Agar Medium ◽

Brown Rot ◽

Initial Population ◽

Monilinia Fructicola ◽

Baseline Sensitivity ◽

Dmi Fungicides ◽

Peach Orchard

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.

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First Reports of Brown Fruit Rot on Sweet Cherry (Prunus avium) and Plum (P. domestica) and Shoot Blight on Apricot (P. armeniaca), Kwanzan Cherry (P. serrulata), and Sweet Cherry (P. avium) Caused by Monilinia laxa in New York, Rhode Island, and Massachusetts

Plant Disease ◽

10.1094/pdis-07-11-0606 ◽

2011 ◽

Vol 95 (12) ◽

pp. 1584-1584 ◽

Cited By ~ 4

Author(s):

K. D. Cox ◽

S. M. Villani ◽

J. J. Raes ◽

J. Freier ◽

H. Faubert ◽

...

Keyword(s):

New York ◽

Rhode Island ◽

Sweet Cherry ◽

Prunus Avium ◽

Pcr Amplification ◽

Stone Fruit ◽

Fruit Rot ◽

Monilinia Laxa ◽

Eastern United States ◽

Shoot Blight

In the eastern United States, Monilinia laxa (Aderh. & Ruhl.) Honey has only been reported on tart cherry in New York (NY) (1). As a result of considerable rain in May of 2009 and 2011, an ornamental planting of Kwanzan cherries in Middletown, Rhode Island (RI), a planting of sweet cherry cvs. Ulster, Hedelfingen, Sam, and Lapins in Lanesboro, Massachusetts (MA), and plantings of apricot cvs. Harcot and Hargrande in Albion, Aurora, and Geneva, NY, and Harogem in Lanesboro, MA developed severe shoot blight (>15 to 100% of first-year shoots). Blighted shoots were wilted with the blight encompassing the distal end and often extending into second-year tissue with a distinct sunken margin. Leaves on symptomatic shoots had flushed, but were blighted and light brown. Blossom spurs were often blighted and gummosis was frequently observed at the base. In these same years, sweet cherry cv. Black Gold in Walworth, NY and plum cv. Stanley in Olcott, NY developed severe fruit rot (35 to 70% incidence). Plantings suffering from fruit rot had fruit lesions that began as pale brown, soft lesions with indiscriminant margins that covered 15 to 85% of the fruit surface area. Many blighted spurs, shoot tissues, and infected fruit were sporulating with tan-to-buff colored conidia produced in chains. From each planting with shoot blight, shoot tips were removed for pathogen isolation. Sections of symptomatic shoots (5 cm long) were surface sterilized in 0.6% NaOCl for 1 min and rinsed in sterile dH20. From plantings displaying blighted spurs or fruit rot, isolation was attempted directly from sporulating tissue. Cross sections of sterilized shoot tissue (3 mm thick) or tufts of sporulation from fruit and spurs were placed on potato dextrose agar amended with 50 μg/ml of streptomycin sulfate. After incubation at 24°C for 5 days, colonies with lobed margins, commonly described for M. laxa (4), were obtained. Several colonies resembling M. fructicola were isolated from all locations, but the majority of isolates from spurs and shoots resembled M. laxa. Conidia from both colony morphotypes were lemon shaped, but as expected, those from putative M. laxa isolates were smaller (10.75 × 12.0 μm) compared with those from putative M. fructicola isolates (15.75 × 18.25 μm) (4). Confirmation of M. laxa was further achieved by PCR amplification of the β-tubulin gene using M. laxa-specific primers as previously described (3). Pathogenicity of M. laxa isolates was proven by inoculating fruit of the stone fruit crop from which they were isolated as previously described (2). Fruit inoculated with M. laxa developed brown, soft sporulating lesions identical to the original observations, while those inoculated with water remained healthy. M. laxa was reisolated from symptomatic shoots and spurs, but not from water-inoculated tissues. The presence of M. laxa has been reported on tart cherries in NY (1), but to our knowledge, this is the first instance of economically devastating shoot blight on apricot in NY and MA, ornamental cherry in RI, and sweet cherry in MA and fruit rot on sweet cherry and plum in NY caused by M. laxa. In wet seasons, stone fruit growers may need to revise their chemical management programs to better prepare for M. laxa epidemics on several stone fruit species. References: (1) K. D. Cox and S. M. Villani. Plant Dis. 94:783, 2010. (2) K. D. Cox and S. M. Villani. Plant Dis. 95:828, 2011. (3) Z. Ma et al. Pest Manag. Sci. 61:449, 2005. J.M. (4) G. C. M. van Leeuwen and H. A. van Kesteren. Can. J. Bot. 76:2042, 1998.

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