Occurrence of powdery mildew caused by Erysiphe betae on chard [Beta vulgaris L. subsp. cicla (L.) Koch] in Greece

2017 ◽  
Vol 99 ◽  
pp. 128-131
Author(s):  
D.J. Vakalounakis ◽  
N. Kavroulakis
2009 ◽  
Vol 99 (4) ◽  
pp. 385-389 ◽  
Author(s):  
Mónica Fernández-Aparicio ◽  
Elena Prats ◽  
Amero A. Emeran ◽  
Diego Rubiales

Beet powdery mildew incited by Erysiphe betae is a serious foliar fungal disease of worldwide distribution causing losses of up to 30%. In the present work, we searched for resistance in a germplasm collection of 184 genotypes of Beta vulgaris including fodder (51 genotypes), garden (60 genotypes), leaf (51 genotypes), and sugar (22 genotypes) beet types. Resistant genotypes were identified in the four beet types under study. In addition, mechanisms underlying resistance were dissected through histological studies. These revealed different resistance mechanisms acting at different fungal developmental stages, i.e., penetration resistance, early and late cell death, or posthaustorial resistance. Most genotypes were able to hamper fungal development at several stages. The later are interesting for breeding aiming to resistance durability. Furthermore, characterization of defense mechanisms will be useful for further cellular and molecular studies to unravel the bases of resistance in this species.


Plant Disease ◽  
2017 ◽  
Vol 101 (1) ◽  
pp. 254-254
Author(s):  
J. H. Joa ◽  
K. C. Seong ◽  
I. Y. Choi ◽  
S. E. Cho ◽  
H. D. Shin

Plant Disease ◽  
2011 ◽  
Vol 95 (4) ◽  
pp. 494-494 ◽  
Author(s):  
L. E. Hanson ◽  
J. M. McGrath

Powdery mildew (Erysiphe polygoni DC [synonym E. betae {Vanha} Weltzien]) affects several different crops of Beta vulgaris, including sugar beet, Swiss chard, and table beet. The disease has been prevalent in many sugar beet-growing areas of the United States since the first major epidemic in beet in 1974 (3). Powdery mildew in the United States was primarily associated with the asexual stage of the pathogen until the perfect stage was found, first in western states such as Idaho and Colorado (2), then in more Midwestern states such as Nebraska, and most recently in North Dakota (1). Similar to North Dakota, powdery mildew has not been a major problem in the Michigan growing area. It does appear sporadically, particularly on sugar beets that have not been sprayed to control other foliar diseases. In 2010, powdery mildew infection on sugar beet was observed in late August in a field in the Saginaw Valley of Michigan. Plants were inspected periodically for the presence of the sexual stage. In early October, sugar beet and Swiss chard plants with heavy powdery mildew infection also were observed at the Michigan State University (MSU) Horticultural Demonstration Gardens in East Lansing and on sugar beet at the MSU Plant Pathology and Botany research farms. On both the Saginaw Valley sugar beet and Swiss chard on the MSU campus, ascomata were observed on a few leaves in mid-October. No ascomata were found on sugar beet at the other two locations. The majority of ascomata were dark brown to black when located, although a few light tan ascomata were observed on the Swiss chard. Ascomata varied from 70 to 100 μm in diameter. Asci contained one to four hyaline or golden yellow ascospores similar to those described in other growing regions on sugar beet (1,2). No ascomata had been detected on powdery mildew-infected sugar beet from either the Saginaw Valley or the MSU research farms the previous two years. These results appear to indicate a spread of the ability to form the perfect stage eastward from the western United States. This may be due to movement of one mating type because E. polygoni has been reported to be heterothallic on some crops (4). The presence of the perfect stage indicates that sexual recombination could occur in E. polygoni on Beta species in Michigan, creating the potential for more rapid development of new strains that might vary in fungicide sensitivity and response to host resistance. References: (1) C. A. Bradley et al. Plant Dis. 91:470, 2007 (2) J. J. Gallian and L. E. Hanson. Plant Dis. 87:200, 2003. (3) E. G. Ruppel. Page 13 in: Compendium of Beet Disease and Insects. E. D. Whitney and J. E. Duffus, eds. The American Phytopathological Society, St. Paul, MN, 1986. (4) C. G. Smith. Trans. Br. Mycol. Soc. 55:355, 1970.


Plant Disease ◽  
2014 ◽  
Vol 98 (10) ◽  
pp. 1429-1429 ◽  
Author(s):  
Y. Zhang ◽  
F. L. Zhang ◽  
P. Cao ◽  
Y. Liu ◽  
K. Liu ◽  
...  

Swiss chard (Beta vulgaris L. subsp. cicla) is a widely planted vegetable in China. From May to June 2013, an outbreak of powdery mildew on Swiss chard cultivar Fangzheng was observed in the commercial fields in Zhoukou city of Henan Province, located in central China. More than 80% of the plants exhibited symptoms of the disease. At the beginning of infection, circular, white, dust-like colonies of powdery mildew occurred mainly on adaxial surfaces of leaves. As the disease progressed, white mycelia covered the foliar parts of plant. No cleistothecia were found on or in collected samples. Upon microscopic evaluation, conidiophores were unbranched with the length of 63 to 126 and width of 7 to 10 μm (n = 50), produced conidia singly, and composed of a cylindrical foot cell followed by one to three short cells. Conidia were colorless, hyaline, ovoid, measured 29 to 40 × 12 to 18 μm (n = 100), lacked fibrosin bodies, and produced germ tubes on the ends of the conidia. The fungus was identified as Erysiphe betae according to the morphological features (1). To verify the identity, the internal transcribed spacer (ITS) region was amplified with the universal primers ITS1 and ITS4 (2) and sequenced. The ITS sequence obtained was assigned as Accession No. KF268348 in GenBank, which showed 100% homogeneity with two ITS sequences of E. betae isolates from UK (DQ164432 and DQ164436). Koch's postulates were conducted by inoculating 15 healthy 5-week-old plants (cv. Fangzheng) with detached infected leaves, which grew in a growth chamber under 22/16°C (day/night), 50% relative humidity, 120 μmol/m2/s light and a 16-h photoperiod. Fifteen non-inoculated plants grew in another growth chamber with the same conditions as control. Symptoms consistent with the infected field plants were observed on the inoculated plants, while no symptoms were found on the control plants. Microscopic observation revealed that the pathogen growing on the inoculated plants was consistent with the morphology of the original fungus. To our knowledge, this is the first report of E. betae infection on Swiss chard in China (3). References: (1) S. Francis. Mol. Plant Pathol. 3:119, 2002. (2) T. J. White et al. Page 315 in: PCR Protocols: A Guide to Methods and Applications. M. A. Innis et al., eds. Academic Press, San Diego, CA, 1990. (3) R. Y. Zheng et al. Page 63 in: Flora Fungorum Sinicorum, Vol. 1, Erysiphales. Science Press, Beijing, 1987.


Plant Disease ◽  
2001 ◽  
Vol 85 (6) ◽  
pp. 627-631 ◽  
Author(s):  
R. T. Lewellen ◽  
J. K. Schrandt

Powdery mildew of sugar beet (Beta vulgaris), caused by Erysiphe polygoni, was introduced into North American in 1974. Since then, chemical control has been needed. Moderate resistance of a slow-mildewing type is known and has been used commercially. High resistance was identified recently in B. vulgaris subsp. maritima accessions WB97 and WB242 and has been backcrossed into sugar beet breeding lines. These enhanced lines were used as sources of powdery mildew resistance to determine the inheritance of resistance. Analyses of segregating testcross families showed that resistance from both sources is inherited as a single, dominant, major gene. The gene symbol Pm is proposed for the resistant allele. The allelism of the resistance from the two wild beet sources was not determined. Pm conditions a high level of resistance, but disease developed on matured leaves late in the season. This late development of mildew on lines and the slow-mildewing trait in susceptible, recurrent lines tended to obfuscate discrete disease ratings.


2019 ◽  
Vol 20 (3) ◽  
pp. 179-179 ◽  
Author(s):  
Thies Marten Heick ◽  
Anne Lisbet Hansen ◽  
Annemarie Fejer Justesen ◽  
Lise Nistrup Jørgensen

Powdery mildew caused by Erysiphe betae is one of the major fungal diseases in sugar beet in Denmark and Sweden. Frequent applications of fungicides mitigate the risk of powdery mildew epidemics and, consequently, reduce yield losses conferred by the disease. So far, mixtures of quinone outside inhibitors (QoIs) and triazoles have provided good efficacy against E. betae in field trials and common farming practice. However, development of fungicide resistance is a real risk, because only a limited number of active ingredients are available for the control of powdery mildew in sugar beet, and several other active ingredients are expected to be banned following reevaluation when the most recent European Union legislation is implemented. The G143A mutation associated with QoI resistance has been previously found in the United States. In this brief, its presence in Europe is reported for the first time. The current finding strongly encourages the adoption of anti-resistance strategies that minimize the spread of QoI resistance in sugar beet powdery mildew. Those strategies should be based on integrated pest management measures, including disease monitoring, the use of resistant cultivars, and the use of biological products. A sole reliance on QoI fungicides for sugar beet powdery mildew control should be avoided.


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