Combination of antagonistic yeasts with two food additives for control of brown rot caused by Monilinia fructicola on sweet cherry fruit

Monilinia fructicola (G. Wint.) Honey is the most important causal agent of brown rot of stone fruits in North America. In July 2010, 20 sweet cherry fruit (Prunus avium) of unknown variety with symptoms resembling brown rot were collected from one commercial orchard in Maryland. Each cherry fruit came from a different tree. Symptoms included necrotic areas up to 10 mm in diameter with brown conidia and conidiophores developing from the infection center. Spores from nine symptomatic fruit collected each from different trees of a single orchard were suspended in sterile water, spread onto the surface of 1% agar plates, and incubated at 22°C. After 12 h, single, germinated spores were transferred onto 9-cm petri dishes with potato dextrose agar (PDA). Nine fungal colonies, each from a different fruit, were investigated in three replicates for cultural characteristics on separate petri dishes containing PDA. They were very similar in morphology and grew 12.4 mm per day on average at 22°C, forming branched, monilioid chains of grayish colonies with concentric rings and little sporulation. Rich sporulation was observed on tomato sauce medium (250 ml tomato sauce and 20 g agar in 750 ml water). The lemon-shaped spores had an average size of 15 × 10 μm, which is consistent with M. fructicola. Two colonies were randomly selected to identify the pathogen to the species level using a PCR technique based on cytochrome b sequence amplifications (2). Resulting gel electrophoresis patterns were consistent with M. fructicola. Koch's postulates were fulfilled by inoculating 15 mature sweet cherry fruits of cv. Bing with a conidial suspension (105 spores/ml) of one of the single-spore isolates from cherry. Fruit were stab-inoculated at a point to a depth of 2 mm using a sterile needle. A 10-μl droplet was placed on each wound; control fruit received sterile water without conidia. After 3 days of incubation at room temperature in airtight plastic bags, the inoculated fruit developed typical brown rot symptoms with lesions that were 20.6 mm in diameter. The developing spores on inoculated fruit were confirmed to be M. fructicola. All control fruit remained healthy. The entire detached fruit experiment was repeated 1 week later. M. fructicola is assumed to be the main causal agent of brown rot of sweet cherry in the northeastern United States, but recent studies show that M. laxa is also causing the disease on sweet cherry in many northeastern states (1). For this reason, it is important to delineate species for accurate disease assessments. This study confirms assumptions that M. fructicola is a causal agent of sweet cherry in Maryland. References: (1) K. D. Cox et al. Plant Dis. 12:1584. 2011. (2) J.-M. Hily et al. Pest Manag. Sci. 67:385, 2011.

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Identification and Etiology of Visible Quiescent Infections of Monilinia fructicola and Botrytis cinerea in Sweet Cherry Fruit

Plant Disease ◽

10.1094/pdis.2000.84.3.328 ◽

2000 ◽

Vol 84 (3) ◽

pp. 328-333 ◽

Cited By ~ 22

Author(s):

J. E. Adaskaveg ◽

H. Förster ◽

D. F. Thompson

Keyword(s):

Botrytis Cinerea ◽

Fungal Pathogens ◽

Sweet Cherry ◽

Brown Rot ◽

Gray Mold ◽

The Other ◽

Monilinia Fructicola ◽

Cherry Orchard ◽

Wetness Period ◽

First Time

Visible quiescent infections were detected as small (<1 mm) necrotic flecks on green cv. Bing cherry fruit and as reddish halos surrounding tannish spots (1 to 2 mm) on immature, yellow-pink cv. Rainier cherry fruit in commercial orchards in California. Monilinia fructicola or Botrytis cinerea, the fungal pathogens causing brown rot and gray mold of cherry fruit, respectively, were isolated from most of the viable infections. M. fructicola was isolated more frequently from quiescent infections than B. cinerea in two years of the study, whereas similar isolation frequencies for both fungi were obtained in the other two years of sampling from one commercial Rainier cherry orchard. Using immature-pink Bing fruit that were inoculated in the laboratory, significantly more visible quiescent infections than active decay were reproduced in 6-, 9-, or 12-h wetness-period treatments after inoculation as compared to 18- or 24-h wetness periods where more active decay developed. Non-visible quiescent infections of M. fructicola or B. cinerea of immature Bing and Rainier fruit collected 2 weeks before harvest were identified on surface-sterilized, paraquat-treated fruit. In both years of the study, significantly more brown rot and gray mold occurred on the surface-sterilized, paraquat-treated fruit than on the non-treated or surface-sterilized fruit, indicating the presence of non-visible quiescent infections by these fungi in cherry fruit. Thus, for the first time, we demonstrated the presence of visible quiescent infections caused by M. fructicola and B. cinerea and we confirmed the occurrence of non-visible quiescent infections in sweet cherry fruit in California.

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First report of brown rot caused by Monilinia fructicola (Winter) Honey on sweet cherry in Turkey

Journal of Plant Pathology ◽

10.1007/s42161-019-00241-6 ◽

2019 ◽

Vol 101 (3) ◽

pp. 773-773 ◽

Cited By ~ 1

Author(s):

Ayşe Uysal ◽

Pervin Kinay-Teksür ◽

Dilek Poyraz

Keyword(s):

Sweet Cherry ◽

Brown Rot ◽

Monilinia Fructicola ◽

First Report

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Effect of Epiphytic Fungi on Brown Rot Blossom Blight and Latent Infections in Sweet Cherry

Plant Disease ◽

10.1094/pdis.1997.81.4.383 ◽

1997 ◽

Vol 81 (4) ◽

pp. 383-387 ◽

Cited By ~ 47

Author(s):

H. P. P. Wittig ◽

K. B. Johnson ◽

J. W. Pscheidt

Keyword(s):

Aureobasidium Pullulans ◽

Sweet Cherry ◽

Brown Rot ◽

Field Trials ◽

Monilinia Fructicola ◽

Dilute Solution ◽

Gliocladium Roseum ◽

Antagonistic Effects ◽

Percent Recovery ◽

Mist Chamber

Antagonistic effects of Aureobasidium pullulans, Epicoccum purpurascens, and Gliocladium roseum on establishment of Monilinia fructicola infections on cv. Royal Anne cherry blossoms were assessed in a mist chamber and under field conditions. Conidia of each fungus were applied to blossoms that were subsequently inoculated with conidia of M. fructicola. Mist chamber experiments on forced blossoms demonstrated that incidence of recovery of M. fructicola from blossoms was significantly reduced (P ≤ 0.05) to similar levels when either E. purpurascens or the fungicide benomyl had been applied 24 h prior to inoculation with M. fructicola. In field trials in 1990, 1991, and 1993, application of E. purpurascens reduced blossom blight relative to nontreated blossoms by 47, 58, and 45%, respectively; whereas application of A. pullulans caused reductions of 54, 13, and 47%, respectively. Comparable reductions in blossom blight for the fungicide iprodione were 80, 95, and 98%, respectively. Latent M. fructicola infections were evaluated by dipping immature green cherries in a dilute solution of the herbicide paraquat. Applications of E. purpurascens and A. pullulans to blossoms reduced the number of latent M. fructicola infections in green cherries by 24 and 48%, respectively, in 1990; 57 and 62%, respectively, in 1991; and 19 and 16%, respectively, in 1993. This compares with reductions of 95, 91, and 17% in 1990, 1991, and 1993, respectively, with the fungicide iprodione. E. purpurascens and G. roseum also were recovered from surface-disinfested, paraquat-dipped cherry fruit. Percent recovery of these fungi was significantly (P ≤ 0.05) higher from treatments where they had been applied to blossoms compared with the nontreated control.

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Interaction of Monoterpenoids, Methyl Jasmonate, and Ca2+ in Controlling Postharvest Brown Rot of Sweet Cherry

HortScience ◽

10.21273/hortsci.35.7.1304 ◽

2000 ◽

Vol 35 (7) ◽

pp. 1304-1307 ◽

Cited By ~ 22

Author(s):

Rong Tsao ◽

Ting Zhou

Keyword(s):

Plant Defense ◽

Methyl Jasmonate ◽

Defense Mechanisms ◽

Sweet Cherry ◽

Prunus Avium ◽

Control Strategies ◽

Brown Rot ◽

Monilinia Fructicola ◽

Alternative Control ◽

Acetate Methyl

The banning of synthetic fungicides for postharvest use on fruits in Canada has prompted a search for alternative control strategies for postharvest brown rot caused by Monilinia fructicola (Wint.) Honey on sweet cherry (Prunus avium L.). Thymol and carvacrol were the two most potent fungicides among the monoterpenoids tested. The brown rot incidences of M. fructicola-inoculated cherry dipped in 1000 μg·mL-1 thymol and carvacrol were 24% and 23%, respectively, compared with 81% for the control. The effects of thymol and carvacrol were not significantly enhanced by the addition of CaCl2 or CaB'y®, a foliar calcium fertilizer. Decco® 282 significantly reduced the activity of thymol. Methyl jasmonate, an elicitor of plant defense mechanisms, did not reduce brown rot by itself, and did not increase the efficacy of thymol and carvacrol when used as an additive in dipping or fumigation experiments. Thymol and carvacrol caused stem browning of cherry fruits in the fumigation experiment, however, 69% and 73%, respectively, of the browning was prevented when methyl jasmonate was used as a co-fumigant. Chemical names used: 5-methyl-2-(1-methylethyl)phenol (thymol); 2-methyl-5-(1-methylethyl)phenol (carvacrol); methyl 3-oxo-2-(2-pentenyl)cyclopentane acetate (methyl jasmonate).

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Genetic diversity assessments of brown rot pathogen Monilinia fructicola based on the six simple sequence repeat loci

Journal of Plant Diseases and Protection ◽

10.1007/s41348-021-00504-4 ◽

2021 ◽

Author(s):

Hakan Guven ◽

Sydney E. Everhart ◽

Rita Milvia De Miccolis Angelini ◽

Hilal Ozkilinc

Keyword(s):

Genetic Diversity ◽

Simple Sequence Repeat ◽

Brown Rot ◽

Monilinia Fructicola ◽

Sequence Repeat ◽

Simple Sequence

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Overexpression of a Redox-Regulated Cutinase Gene, MfCUT1, Increases Virulence of the Brown Rot Pathogen Monilinia fructicola on Prunus spp.

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-23-2-0176 ◽

2010 ◽

Vol 23 (2) ◽

pp. 176-186 ◽

Cited By ~ 28

Author(s):

Miin-Huey Lee ◽

Chiu-Min Chiu ◽

Tatiana Roubtsova ◽

Chien-Ming Chou ◽

Richard M. Bostock

Keyword(s):

Gene Expression ◽

Redox Regulation ◽

Brown Rot ◽

Gus Expression ◽

Apple Fruit ◽

Gus Activity ◽

Monilinia Fructicola ◽

Gus Reporter ◽

Flanking Regions ◽

Prunus Spp

A 4.5-kb genomic DNA containing a Monilinia fructicola cutinase gene, MfCUT1, and its flanking regions were isolated and characterized. Sequence analysis revealed that the genomic MfCUT1 carries a 63-bp intron and a promoter region with several transcription factor binding sites that may confer redox regulation of MfCUT1 expression. Redox regulation is indicated by the effect of antioxidants, shown previously to inhibit MfCUT1 gene expression in cutin-induced cultures, and in the present study, where H2O2 enhanced MfCUT1 gene expression. A β-glucuronidase (GUS) reporter gene (gusA) was fused to MfCUT1 under the control of the MfCUT1 promoter, and this construct was then used to generate an MfCUT1-GUS strain by Agrobacterium spp.-mediated transformation. The appearance of GUS activity in response to cutin and suppression of GUS activity by glucose in cutinase-inducing medium verified that the MfCUT1-GUS fusion protein was expressed correctly under the control of the MfCUT1 promoter. MfCUT1-GUS expression was detected following inoculation of peach and apple fruit, peach flower petals, and onion epidermis, and during brown rot symptom development on nectarine fruit at a relatively late stage of infection (24 h postinoculation). However, semiquantitative reverse-transcriptase polymerase chain reaction provided sensitive detection of MfCUT1 expression within 5 h of inoculation in both almond and peach petals. MfCUT1-GUS transformants expressed MfCUT1 transcripts at twice the level as the wild type and caused more severe symptoms on Prunus flower petals, consistent with MfCUT1 contributing to the virulence of M. fructicola.

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First Report of Brown Rot Caused by Monilinia fructicola Affecting Peach Orchards in Slovenia

Plant Disease ◽

10.1094/pdis-94-9-1166a ◽

2010 ◽

Vol 94 (9) ◽

pp. 1166-1166 ◽

Cited By ~ 15

Author(s):

A. Munda ◽

M. Viršček Marn

Keyword(s):

Prunus Persica ◽

Brown Rot ◽

Fruit Rot ◽

Morphological Identification ◽

Monilinia Fructicola ◽

Conidial Suspension ◽

Stone Fruits ◽

The European Union ◽

First Report ◽

Representative Isolate

Monilinia fructicola, the causal agent of brown rot, is a destructive fungal pathogen that affects mainly stone fruits (Prunoideae). It causes fruit rot, blossom wilt, twig blight, and canker formation and is common in North and South America, Australia, and New Zealand. M. fructicola is listed as a quarantine pathogen in the European Union and was absent from this region until 2001 when it was detected in France. In August 2009, mature peaches (Prunus persica cv. Royal Glory) with brown rot were found in a 5-year-old orchard in Goriška, western Slovenia. Symptoms included fruit lesions and mummified fruits. Lesions were brown, round, rapidly extending, and covered with abundant gray-to-buff conidial tufts. The pathogen was isolated in pure culture and identified based on morphological and molecular characters. Colonies on potato dextrose agar (PDA) incubated at 25°C in darkness had an average daily growth rate of 7.7 mm. They were initially colorless and later they were light gray with black stromatal plates and dense, hazel sporogenous mycelium. Colony margins were even. Sporulation was abundant and usually developed in distinct concentric zones. Limoniform conidia, produced in branched chains, measured 10.1 to 17.7 μm (mean = 12.1 μm) × 6.2 to 8.6 μm (mean = 7.3 μm) on PDA. Germinating conidia produced single germ tubes whose mean length ranged from 251 to 415 μm. Microconidia were abundant, globose, and 3 μm in diameter. Morphological characters resembled those described for M. fructicola (1). Morphological identification was confirmed by amplifying genomic DNA of isolates with M. fructicola species-specific primers (2–4). Sequence of the internal transcribed spacer (ITS) region (spanning ITS1 and ITS 2 plus 5.8 rDNA) of a representative isolate was generated using primers ITS1 and ITS4 and deposited in GenBank (Accession No. GU967379). BLAST analysis of the 516-bp PCR product revealed 100% identity with several sequences deposited for M. fructicola in NCBI GenBank. Pathogenicity was tested by inoculating five mature surface-sterilized peaches with 10 μl of a conidial suspension (104 conidia ml–1) obtained from one representative isolate. Sterile distilled water was used as a control. Peaches were wounded prior to inoculation. After 5 days of incubation at room temperature and 100% relative humidity, typical brown rot symptoms developed around the inoculation point, while controls showed no symptoms. M. fructicola was reisolated from lesion margins. Peach and nectarine orchards in a 5-km radius from the outbreak site were surveyed in September 2009 and M. fructicola was confirmed on mummified fruits from seven orchards. The pathogen was not detected in orchards from other regions of the country, where only the two endemic species M. laxa and M. fructigena were present. To our knowledge, this is the first report of M. fructicola associated with brown rot of stone fruits in Slovenia. References: (1) L. R. Batra. Page 106 in: World Species of Monilinia (Fungi): Their Ecology, Biosystematics and Control. J. Cramer, Berlin, 1991. (2) M.-J. Côté et al. Plant Dis. 88:1219, 2004. (3) K. J. D. Hughes et al. EPPO Bull. 30:507, 2000. (4) R. Ioos and P. Frey. Eur. J. Plant Pathol. 106:373, 2000.

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