scholarly journals First Report of Rhizomania Disease of Sugar Beet Caused by Beet necrotic yellow vein virus in the Great Lakes Production Region

Plant Disease ◽  
2003 ◽  
Vol 87 (2) ◽  
pp. 201-201 ◽  
Author(s):  
William M. Wintermantel ◽  
Teresa Crook ◽  
Ralph Fogg

Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV) and vectored by the soilborne fungus Polymyxa betae Keskin, is one of the most economically damaging diseases affecting sugar beet (Beta vulgaris L.). The virus likely originated in Europe and was first identified in California in 1983 (1). It has since spread among American sugar beet production regions in spite of vigorous sanitation efforts, quarantine, and disease monitoring (3). In the fall of 2002, mature sugar beet plants exhibiting typical rhizomania root symptoms, including proliferation of hairy roots, vascular discoloration, and some root constriction (2) were found in several fields scattered throughout central and eastern Michigan. Symptomatic beets were from numerous cultivars, all susceptible to rhizomania. Two to five sugar beet root samples were collected from each field and sent to the USDA-ARS in Salinas, CA for analysis. Hairy root tissue from symptomatic plants was used for mechanical inoculation of indicator plants. Mechanical inoculation produced necrotic lesions on Chenopodium quinoa and systemic infection of Beta vulgaris ssp. macrocarpa, both typical of BNYVV and identical to control inoculations with BNYVV. Symptomatic sugar beet roots were washed and tested using double antibody sandwich-enzyme linked immunosorbent assay (DAS-ELISA) for the presence of BNYVV using standard procedures and antiserum specific for BNYVV (3). Sugar beet roots were tested individually, and samples were considered positive when absorbance values were at least three times those of greenhouse-grown healthy sugar beet controls. Samples were tested from 16 fields, with 10 confirmed positive for BNYVV. Positive samples had mean absorbance values ranging from 0.341 to 1.631 (A405nm) after 30 min. The mean healthy control value was 0.097. Fields were considered positive if one beet tested positive for BNYVV, but in most cases, all beets tested from a field were uniformly positive or uniformly negative. In addition, soil-baiting experiments were conducted on seven of the fields. Sugar beet seedlings were grown in soil mixed with equal parts of sand for 6 weeks and were subsequently tested using DAS-ELISA for BNYVV. Results matched those of the root sampling. Fields testing positive for BNYVV were widely dispersed within a 100 square mile (160 km2) area including portions of Gratiot, Saginaw, Tuscola, and Sanilac counties in the central and eastern portions of the Lower Peninsula of Michigan. The confirmation of rhizomania in sugar beet from the Great Lakes Region marks the last major American sugar beet production region to be diagnosed with rhizomania disease, nearly 20 years after its discovery in California (1). In 2002, there were approximately 185,000 acres (approximately 75,00 ha) of sugar beet grown in the Great Lakes Region, (Michigan, Ohio, and southern Ontario, Canada). The wide geographic distribution of infested fields within the Michigan growing area suggests the entire region should monitor for symptoms, increase rotation to nonhost crops, and consider planting rhizomania resistant sugar beet cultivars to infested fields. References:(1) J. E. Duffus et al. Plant Dis. 68:251, 1984. (2) J. E. Duffus. Rhizomania. Pages 29–30 in: Compendium of Beet Diseases and Insects, E. D. Whitney and J. E. Duffus eds. The American Phytopathological Society, St. Paul, MN, 1986. (3) G. C. Wisler et al. Plant Dis. 83:864, 1999.

Agriculture ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 956
Author(s):  
Thomas M. Lange ◽  
Martin Wutke ◽  
Lisa Bertram ◽  
Harald Keunecke ◽  
Friedrich Kopisch-Obuch ◽  
...  

The Beet necrotic yellow vein virus (BNYVV) causes rhizomania in sugar beet (Beta vulgaris L.), which is one of the most destructive diseases in sugar beet worldwide. In breeding projects towards resistance against BNYVV, the enzyme-linked immunosorbent assay (ELISA) is used to determine the virus concentration in plant roots and, thus, the resistance levels of genotypes. Here, we present a simulation study to generate 10,000 small samples from the estimated density functions of ELISA values from susceptible and resistant sugar beet genotypes. We apply receiver operating characteristic (ROC) analysis to these samples to optimise the cutoff values for sample sizes from two to eight and determine the false positive rates (FPR), true positive rates (TPR), and area under the curve (AUC). We present, furthermore, an alternative approach based upon Bayes factors to improve the decision procedure. The Bayesian approach has proven to be superior to the simple cutoff approach. The presented results could help evaluate or improve existing breeding programs and help design future selection procedures based upon ELISA. An R-script for the classification of sample data based upon Bayes factors is provided.


2003 ◽  
Vol 69 (4) ◽  
pp. 2356-2360 ◽  
Author(s):  
Alexandre Meunier ◽  
Jean-François Schmit ◽  
Arnaud Stas ◽  
Nazli Kutluk ◽  
Claude Bragard

ABSTRACT Three soilborne viruses transmitted by Polymyxa betae KESKIN in sugar beet have been described: Beet necrotic yellow vein virus (BNYVV), the agent of rhizomania, Beet soilborne virus (BSBV), and Beet virus Q (BVQ). A multiplex reverse transcription-PCR technique was developed to simultaneously detect BNYVV, BSBV, and BVQ, together with their vector, P. betae. The detection threshold of the test was up to 128 times greater than that of an enzyme-linked immunosorbent assay. Systematic association of BNYVV with one or two different pomoviruses was observed. BVQ was detected in samples from Belgium, Bulgaria, France, Germany, Hungary, Italy, Sweden, and The Netherlands but not in samples from Turkey.


Plant Disease ◽  
2002 ◽  
Vol 86 (1) ◽  
pp. 72-72 ◽  
Author(s):  
J. J. Gallian ◽  
W. M. Wintermantel ◽  
P. B. Hamm

Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV) and vectored by the soilborne fungus, Polymyxa betae Keskin, is one of the most economically damaging diseases affecting sugar beet (Beta vulgaris L.) worldwide and has been found in most sugar beet-growing areas of the United States (2). During harvest in October 2000, sugar beet plants exhibiting typical symptoms of rhizomania (1) were found in a field near Paterson, WA. Sugar beet had been planted in the field in 1999 and 2000, but prior to this, the field had not been planted with sugar beet for approximately 20 years. Symptomatic roots from the field exhibited stunting, vascular discoloration, and proliferation of lateral rootlets. Leaves of affected plants were chlorotic. Four soil samples were taken from symptomatic areas of the field and diluted with an equal amount of sterile sand. Seeds of rhizomania-susceptible sugar beet cv. Beta 8422 were planted in the soil and sand mix and maintained in a controlled environment at 24°C and 12 h of daylight at one location and in the greenhouse at another. After 8 weeks, enzyme-linked immunosorbent assay (ELISA) was performed on roots of plants grown at each location. Triple-antibody sandwich (TAS) ELISA (Agdia, Inc., Elkhart, IN) was conducted at the University of Idaho, Twin Falls, ID and double-antibody sandwich (DAS) ELISA was performed at USDA-ARS, Salinas, CA, with antiserum specific for BNYVV (2). Two of four samples were positive for BNYVV in the ELISA tests at both locations based on absorbance values at least three times those of healthy controls. TAS-ELISA tests were conducted on roots collected in July 2001 from a field in Washington, 12.9 km from the first field, as well as from a field across the Columbia River near Boardman, OR. Samples from both fields tested positive for BNYVV. All three fields are within 24 km of one another. Four additional fields have subsequently been confirmed to be infected with BNYVV in this region, based on symptomology and ELISA. There are approximately 3,240 ha of sugar beet grown in the region, and growers have been advised as a result of this confirmation to plant resistant cultivars and increase the sugar beet rotation interval with nonhost crops to a minimum of 4 years. References: (1) J. E. Duffus. Rhizomania. Pages 29–30 in: Compendium of Beet Diseases and Insects. E. D. Whitney and J. E. Duffus, eds. The American Phytopathological Society, St. Paul, MN, 1986. (2) G. C. Wisler et al. Plant Dis. 83:864, 1999.


Plant Disease ◽  
2003 ◽  
Vol 87 (10) ◽  
pp. 1170-1175 ◽  
Author(s):  
G. C. Wisler ◽  
R. T. Lewellen ◽  
J. L. Sears ◽  
J. W. Wasson ◽  
H.-Y. Liu ◽  
...  

Soils naturally infested with cultures of aviruliferous Polymyxa betae and viruliferous P. betae carrying two sugar beet benyviruses, Beet necrotic yellow vein virus (BNYVV) and Beet soilborne mosaic virus (BSBMV), alone and in combination, were compared with noninfested soil for their effects on seedling emergence, plant fresh weight, and virus content as measured by enzyme-linked immunosorbent assay (ELISA). Studies examined sugar beet with and without resistance to the disease rhizomania, caused by BNYVV. The Rz gene, conferring resistance to BNYVV, did not confer resistance to BSBMV. BSBMV ELISA values were significantly higher in single infections than in mixed infections with BNYVV, in both the rhizomania-resistant and -susceptible cultivars. In contrast, ELISA values of BNYVV were high (8 to 14 times the healthy mean) in single and mixed infections in the rhizomania-susceptible cultivar, but were low (approximately three times the healthy mean) in the rhizomania-resistant cultivar. Results indicate BNYVV may suppress BSBMV in mixed infections, even in rhizomania-resistant cultivars in which ELISA values for BNYVV are extremely low. Soils infested with P. betae, and with one or both viruses, showed significantly reduced fresh weight of seedlings, and aviruliferous P. betae significantly decreased sugar beet growth in assays.


Plant Disease ◽  
2008 ◽  
Vol 92 (7) ◽  
pp. 1043-1047 ◽  
Author(s):  
H.-Y. Liu ◽  
R. T. Lewellen

Rhizomania, a serious disease of sugar beet (Beta vulgaris), is caused by Beet necrotic yellow vein virus (BNYVV). Resistance allele Rz1 has been widely incorporated into commercial cultivars. Recently, resistance-breaking isolates of BNYVV (RB-BNYVV) were identified and characterized. When the occurrence of RB-BNYVV was surveyed throughout the sugar-beet-growing areas in the United States, most soil samples contained Beet oak-leaf virus (BOLV) as well. BNYVV and BOLV often occurred in the same field and sometimes in the same sugar beet plant. The possibility of interactions between these two Polymyxa betae-transmitted sugar beet viruses was tested. Plants grown in soils infested with aviruliferous P. betae or carrying RB-BNYVV and BOLV, alone and in combination, were compared with plants grown in noninfested soil for differences in plant fresh weight and virus content as measured by enzyme-linked immunosorbent assay (ELISA). Rz1 and Rz2 resistance genes that condition resistance to BNYVV did not confer resistance to BOLV. BNYVV ELISA values were significantly higher in single infections than in mixed infections with BOLV in both the rhizomania-resistant and -susceptible cultivars. In contrast, ELISA values of BOLV were not significantly different between single and mixed infections in both the rhizomania-resistant and -susceptible cultivars. Results indicate that BOLV may suppress BNYVV in mixed infections. Soils infested with P. betae significantly reduced fresh weight of sugar beet seedlings regardless of whether they were with or without one or both viruses or resistance genes.


2008 ◽  
Vol 89 (5) ◽  
pp. 1314-1323 ◽  
Author(s):  
Soutaro Chiba ◽  
Masaki Miyanishi ◽  
Ida Bagus Andika ◽  
Hideki Kondo ◽  
Tetsuo Tamada

The RNA3-encoded p25 protein of beet necrotic yellow vein virus (BNYVV) is responsible for the production of rhizomania symptoms of sugar beet roots (Beta vulgaris subsp. vulgaris). Here, it was found that the presence of the p25 protein is also associated with the resistance response in rub-inoculated leaves of sugar beet and wild beet (Beta vulgaris subsp. maritima) plants. The resistance phenotype displayed a range of symptoms from no visible lesions to necrotic or greyish lesions at the inoculation site, and only very low levels of virus and viral RNA accumulated. The susceptible phenotype showed large, bright yellow lesions and developed high levels of virus accumulation. In roots after Polymyxa betae vector inoculation, however, no drastic differences in virus and viral RNA accumulation levels were found between plants with susceptible and resistant phenotypes, except at an early stage of infection. There was a genotype-specific interaction between BNYVV strains and two selected wild beet lines (MR1 and MR2) and sugar beet cultivars. Sequence analysis of natural BNYVV isolates and site-directed mutagenesis of the p25 protein revealed that 3 aa residues at positions 68, 70 and 179 are important in determining the resistance phenotype, and that host-genotype specificity is controlled by single amino acid changes at position 68. The mechanism of the occurrence of resistance-breaking BNYVV strains is discussed.


2020 ◽  
Vol 112 ◽  
pp. 101520
Author(s):  
Kimberly M. Webb ◽  
William M. Wintermantel ◽  
Lisa Wolfe ◽  
Linxing Yao ◽  
Laura Jenkins Hladky ◽  
...  

Plant Disease ◽  
1999 ◽  
Vol 83 (9) ◽  
pp. 864-870 ◽  
Author(s):  
G. C. Wisler ◽  
R. T. Lewellen ◽  
J. L. Sears ◽  
H.-Y. Liu ◽  
J. E. Duffus

Levels of beet necrotic yellow vein virus (BNYVV), as measured by triple-antibody sandwich-enzyme-linked immunosorbent assay (TAS-ELISA), were compared with biological evaluations in representative commercial and experimental sugar beet cultivars developed for production in the United States and ranging in their reactions to rhizomania from uniformly susceptible to highly resistant. TAS-ELISA was specific for BNYVV and did not react with related soilborne sugar beet viruses. Differences in absorbance (A405nm) values measured in eight cultivars closely correlated with the dosage and frequency of the Rz allele, which conditions resistance to BNYVV. A diploid (Rzrz) hybrid had a significantly lower absorbance value (less virus) than a similar triploid (Rzrzrz) hybrid. Cultivars that segregated (Rzrz:rzrz) had higher absorbance values than uniformly resistant (Rzrz) hybrids, as was expected. For all cultivars, absorbance values decreased as the season progressed. Absorbance value was significantly positively correlated with rhizomania disease index score and negatively correlated with individual root weight, plot root weight, and sugar yield. This information should be useful in resistance-breeding and -evaluation programs and in the sugar industry when considering cultivar choice, inoculum production, and future crop rotations.


Plant Disease ◽  
2007 ◽  
Vol 91 (7) ◽  
pp. 847-851 ◽  
Author(s):  
H.-Y. Liu ◽  
R. T. Lewellen

Beet necrotic yellow vein virus (BNYVV) is the causal agent of rhizomania in sugar beet (Beta vulgaris). The virus is transmitted by the plasmodiophorid Polymyxa betae. The disease is controlled primarily by the use of partially resistant cultivars. During 2003 and 2004 in the Imperial Valley of California, partially resistant sugar beet cultivars with Rz1 allele seemed to be compromised. Field trials at Salinas, CA have confirmed that Rz1 has been defeated by resistance-breaking isolates. Distinct BNYVV isolates have been identified from these plants. Rhizomania-infested sugar beet fields throughout the United States were surveyed in 2004–05. Soil surveys indicated that the resistance-breaking isolates not only existed in the Imperial Valley and San Joaquin Valley of California but also in Colorado, Idaho, Minnesota, Nebraska, and Oregon. Of the soil samples tested by baited plant technique, 92.5% produced infection with BNYVV in ‘Beta 6600’ (rz1rz1rz1), 77.5% in ‘Beta 4430R’ (Rz1rz1), 45.0% in ‘Beta G017R’ (Rz2rz2), and 15.0% in ‘KWS Angelina’ (Rz1rz1+Rz2rz2). Analyses of the deduced amino acid sequence of coat protein and P-25 protein of resistance-breaking BNYVV isolates revealed the high percentage of identity with non-resistance-breaking BNYVV isolates (99.9 and >98.0%, respectively). The variable amino acids in P-25 proteins were located at the residues of 67 and 68. In the United States, the two amino acids found in the non-resistance-breaking isolates were conserved (AC). The resistance-breaking isolates were variable including, AF, AL, SY, VC, VL, and AC. The change of these two amino acids cannot be depended upon to differentiate resistance-breaking and non-resistance-breaking isolates of BNYVV.


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