BREEDING FOR BROWN ROT (MONILINIA FRUCTICOLA) RESISTANCE IN CLINGSTONE PEACH WITH EMPHASIS ON THE ROLE OF FRUIT PHENOLICS

1998 ◽  
pp. 161-170 ◽  
Author(s):  
T.M. Gradziel ◽  
M.A. Thorpe ◽  
R.M. Bostock ◽  
S. Wilcox
Keyword(s):  
Brown Rot ◽  
Monilinia Fructicola ◽  
Fruit Phenolics

scholarly journals Preservation of Monilinia fructicola Genotype Diversity Within Fungal Cankers

Plant Disease ◽  
2019 ◽  
Vol 103 (3) ◽  
pp. 526-530 ◽  
Author(s):  
Madeline E. Dowling ◽  
William C. Bridges ◽  
Brodie M. Cox ◽  
Tommy Sroka ◽  
Jennifer R. Wilson ◽  
...  
Keyword(s):  
Management Strategies ◽  
Fungal Spores ◽  
Brown Rot ◽  
Fruit Rot ◽  
Monilinia Fructicola ◽  
Reproductive Tissue ◽  
Inoculum Source ◽  
Storage Structures ◽  
Simple Sequence

Monilinia fructicola is a destructive pathogen causing brown rot on stone fruits worldwide. Though it is best known as a fruit rot pathogen, M. fructicola also causes blossom blight and, subsequently, twig cankers in the spring. Orchard management strategies often overlook cankers as an inoculum source, though they are an inoculum source of both blossom and fruit infections. In this study, we analyzed the role of cankers as storage structures for diverse genotypes of M. fructicola, examining whether multiple genotypes can be transmitted from blossom to canker. Fungal spores from blossoms, and 2 months later from their corresponding cankers, were collected from a conventional and an unsprayed orchard in 2015 and 2016. Simple sequence repeat markers were used to genotype 10 to 20 single spores from each of four blossom/canker pairs per orchard. Individual blossoms and cankers were detected containing up to four and five genotypes, respectively. The average number of genotypes in blossoms and corresponding cankers were not significantly different (P = 0.690) across both years and farms, showing that a bottleneck for genetic diversity was not generated during the transition from blossom to canker. The average number of genotypes unique to blossom or canker was not significantly different (P = 0.569) and no significant effect of farm (P = 0.961) or year (P = 0.520) was observed, although blossoms had a numerically greater number of unique genotypes in both cases. In conclusion, a single blossom may be infected by one or more genotypes of M. fructicola, and this diversity is being preserved in the corresponding canker. This information implicates M. fructicola cankers as diversity storehouses, and may also apply to other Monilinia spp. and fungal diseases that initiate in reproductive tissue.

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

2010 ◽  
Vol 23 (2) ◽  
pp. 176-186 ◽  
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.

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

Plant Disease ◽  
2010 ◽  
Vol 94 (9) ◽  
pp. 1166-1166 ◽  
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.

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

2003 ◽  
Vol 69 (12) ◽  
pp. 7145-7152 ◽  
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.

scholarly journals Effect of Temperature on the Discharge and Germination of Ascospores by Apothecia of Monilinia fructicola

Plant Disease ◽  
1998 ◽  
Vol 82 (2) ◽  
pp. 195-202 ◽  
Author(s):  
Chuanxue Hong ◽  
Themis J. Michailides
Keyword(s):  
Management Strategies ◽  
Brown Rot ◽  
Effect Of Temperature ◽  
Monilinia Fructicola ◽  
Stone Fruits ◽  
Warning Systems ◽  
Fresno County ◽  
Ascospore Germination ◽  
Daily Discharge ◽  
Germ Tubes

Naturally growing apothecia of Monilinia fructicola were collected from two commercial plum orchards near Reedley and Sanger, both in Fresno County, California. Ascospore discharges from 90 (1996) and 86 (1997) apothecia were monitored individually using spore traps at four constant temperatures. The period of discharge decreased as temperature increased from 10 to 25°C. However, daily discharge increased as temperature increased from 10 to 15°C and remained high at 20 and 25°C. The greatest discharge occurred with apothecia at 15°C, followed by those incubated at 20, 10, and 25°C. The germination of ascospores of M. fructicola and the length of germ tubes increased as temperature increased from 7 to 15°C; however, increasing temperatures above 15°C did not increase either ascospore germination or length of germ tubes. This information may help in the development of warning systems and management strategies for brown rot blossom blight of stone fruits.

scholarly journals Factors Affecting Latent Infection of Prune Fruit by Monilinia fructicola

2001 ◽  
Vol 91 (9) ◽  
pp. 864-872 ◽  
Author(s):  
Yong Luo ◽  
Themis J. Michailides
Keyword(s):  
Growth Stage ◽  
Latent Infection ◽  
Developmental Stages ◽  
Seasonal Pattern ◽  
Brown Rot ◽  
Effect Of Temperature ◽  
Monilinia Fructicola ◽  
Inoculum Concentration ◽  
Factors Affecting ◽  
Commercial Harvest

Experiments were conducted in three prune orchards in California. In each orchard, inoculations with Monilinia fructicola, the causal agent of brown rot of stone fruits, were performed on branches of trees at bloom and fruit developmental stages. Five inoculum concentrations were used in each inoculation. Six and four wetness durations were created for each inoculum concentration at bloom and fruit developmental stages, respectively. Fruit were harvested 3 weeks before commercial harvest. The overnight freezing incubation technique was used to promote sporulation and to determine incidence of latent infection (ILI) of fruit brown rot. No differences in ILI among locations were found. A seasonal pattern of bloom and fruit susceptibility to latent infection was determined. Susceptibility to latent infection at bloom stage was at a moderate level and increased to reach the highest level at pit hardening stage. Subsequently, fruit susceptibility to latent infection decreased, reaching the lowest level in early June at embryo growth stage. Thereafter, the susceptibility increased again with fruit development and maturity until harvest. Linear relationships between ILI and inoculum concentration were obtained for most combinations of growth stage and wetness duration. Incidence of latent infection increased linearly with increased wetness duration at bloom stage and increased exponentially with increased wetness duration at early and late fruit developmental stages. The optimum temperatures for latent infection at pit hardening stage ranged from 14 to 18°C, but the effect of temperature on latent infection was reduced at resistant stages. The temperature range favorable to latent infection varied for different wetness durations.

Brown rot of stone fruits on the Murrumbidgee Irrigation Areas. II. Aetiology of the disease in Trevatt apricot trees

1969 ◽  
Vol 20 (2) ◽  
pp. 317 ◽  
Author(s):  
PF Kable
Keyword(s):  
Brown Rot ◽  
Economic Importance ◽  
Fruit Rot ◽  
Monilinia Fructicola ◽  
Stone Fruits

Blossom blight is of economic importance in apricots on the Murrumbidgee Irrigation Areas (MIA), but fruit rot is not. Monilinia fructicola generally does not overwinter effectively in apricot trees in the MIA, the inocula for primary infections coming from nearby peach plantations. Blighted blossoms in apricot trees, which flower a week before peaches, may provide inoculum for blighting of flowers in the latter crop. In apricot trees, unlike peach, there is a continuous infection chain from flowering till harvest. Inoculum may pass from apricot to peach in December and January, thus bridging a gap in the infection chain in peach. The infection chain in apricot is described. Latent and quiescent infections were observed. The implications of the exchange of inoculum between peach and apricot are discussed.

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