scholarly journals Pathogenetic roles of beet necrotic yellow vein virus RNA5 in the exacerbation of symptoms and yield reduction, development of scab‐like symptoms, and Rz1 ‐resistance breaking in sugar beet

2020 ◽  
Vol 70 (1) ◽  
pp. 219-232 ◽  
Author(s):  
Tetsuo Tamada ◽  
Hirokatsu Uchino ◽  
Toshimi Kusume ◽  
Minako Iketani‐Saito ◽  
Sotaro Chiba ◽  
...  
Keyword(s):  
Sugar Beet ◽  
Yellow Vein ◽  
Yield Reduction ◽  
Resistance Breaking ◽  
Exacerbation Of Symptoms

scholarly journals Distribution and Molecular Characterization of Resistance-Breaking Isolates of Beet necrotic yellow vein virus in the United States

Plant Disease ◽  
2007 ◽  
Vol 91 (7) ◽  
pp. 847-851 ◽  
Author(s):  
H.-Y. Liu ◽  
R. T. Lewellen
Keyword(s):  
United States ◽  
Amino Acids ◽  
Sugar Beet ◽  
The United States ◽  
Field Trials ◽  
Yellow Vein ◽  
Polymyxa Betae ◽  
Imperial Valley ◽  
Resistance Breaking ◽  
Soil Surveys

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.

scholarly journals The Evolutionary History of Beet necrotic yellow vein virus Deduced from Genetic Variation, Geographical Origin and Spread, and the Breaking of Host Resistance

2011 ◽  
Vol 24 (2) ◽  
pp. 207-218 ◽  
Author(s):  
Soutaro Chiba ◽  
Hideki Kondo ◽  
Masaki Miyanishi ◽  
Ida Bagus Andika ◽  
Chenggui Han ◽  
...  
Keyword(s):  
Sugar Beet ◽  
Host Resistance ◽  
Evolutionary History ◽  
Sequence Variation ◽  
Geographical Origin ◽  
Geographical Location ◽  
Yellow Vein ◽  
Resistance Breaking ◽  
History Of ◽  
Report Analysis

Beet necrotic yellow vein virus (BNYVV) is an economically important pathogen of sugar beet and has been found worldwide, probably as the result of recent worldwide spread. The BNYVV genome consists of four or five RNA components. Here, we report analysis of sequence variation in the RNA3-p25, RNA4-p31, RNA2-CP, and RNA5-p26 genes of 73 worldwide isolates. The RNA3-p25 gene encodes virulence and avirulence factors. These four sets of gene sequences each fell into two to four groups, of which the three groups of p25 formed eight subgroups with different geographical distributions. Each of these subgroup isolates (strains) could have arisen from four original BNYVV population and their mixed infections. The genetic diversity for BNYVV was relatively small. Selection pressure varied greatly depending on the BNYVV gene and geographical location. Isolates of the Italy strain, in which p25 was subject to the strongest positive selection, were able to overcome the Rz1-host resistance gene to differing degrees, whereas other geographically limited strains could not. Resistance-breaking variants were generated by p25 amino acid changes at positions 67 and 68. Our studies suggest that BNYVV originally evolved in East Asia and has recently become a pathogen of cultivated sugar beet followed by the emergence of new resistance-breaking variants.

scholarly journals Suppression of Resistance-Breaking Beet necrotic yellow vein virus Isolates by Beet oak-leaf virus in Sugar Beet

Plant Disease ◽  
2008 ◽  
Vol 92 (7) ◽  
pp. 1043-1047 ◽  
Author(s):  
H.-Y. Liu ◽  
R. T. Lewellen
Keyword(s):  
Sugar Beet ◽  
Resistance Genes ◽  
The United States ◽  
Yellow Vein ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mixed Infections ◽  
Polymyxa Betae ◽  
Fresh Weight ◽  
Resistance Breaking ◽  
Leaf Virus

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.

Breeding and usage of sugar beet cultivars and hybrids resistant to sugar beet nematode Heterodera schachtii

2015 ◽  
Vol 2 (1) ◽  
pp. 12-22 ◽  
Author(s):  
L. Pylypenko ◽  
K. Kalatur
Keyword(s):  
Sugar Beet ◽  
Sugar Content ◽  
Production Capacity ◽  
Nematode Resistance ◽  
Control Measures ◽  
Heterodera Schachtii ◽  
Yield Reduction ◽  
Agricultural Practice ◽  
Germplasm Exchange ◽  
Good Agricultural Practice

Heterodera schachtii Schmidt, 1871 is one of the most economically important pests of sugar beet (Beta vulgaris L.) worldwide. It is also widespread in most sugar beet growing regions in Ukraine causing serious yield reduction and decreasing sugar content of sugar beet in infested fi elds. An advanced parasitic strategy of H. schachtii is employed to support nematode growth, reproduction and harmfulness. In intensive agriculture systems the nematode control measures heavily rely on nematicides and good agricultural practice (crop rota- tion in the fi rst place). But alternative strategies based on nematode resistant sugar beet cultivars and hybrids are required as none of nematicides approved for the open fi eld application are registered in Ukraine. Here we review the achievements and problems of breeding process for H. schachtii resistance and provide the results of national traditional breeding program. Since the beginning of 1980s fi ve sugar beet cultivars (Verchnyatskyi 103, Yaltuschkivska 30, Bilotcerkivska 45, BTs-40 and Yuvileynyi) and seventeen lines partly resistant or toler- ant to H. schachtii have been obtained throughout targeted crossing and progenies assessment in the infested fi elds. The further directions for better utilization of genetic sources for nematode resistance presented in na- tional gene bank collection are emphasized. There is a need for more accurate identifi cation of resistance genes, broader application of reliable molecular markers (suitable for marker-assisted selection of nematode resistant plants in the breeding process) and methods for genetic transformation of plants. Crop cash value and national production capacity should drive the cooperation in this fi eld. Knowledge as well as germplasm exchange are thereby welcomed that can benefi t breeding progress at national and international level.

Beet necrotic yellow vein virus genome reassortments in a resistant sugar beet variety showing–in a small area in France–strong rhizomania symptoms

2009 ◽  
Vol 116 (1) ◽  
pp. 7-9 ◽  
Author(s):  
R. Koenig ◽  
B. Holtschulte ◽  
G. Deml ◽  
P. Lüddecke ◽  
S. Schuhmann ◽  
...  
Keyword(s):  
Sugar Beet ◽  
Small Area ◽  
Virus Genome ◽  
Yellow Vein ◽  
Sugar Beet Variety

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
Keyword(s):  
Sugar Beet ◽  
Great Lakes ◽  
Beta Vulgaris ◽  
Yellow Vein ◽  
Enzyme Linked Immunosorbent Assay ◽  
Great Lakes Region ◽  
Polymyxa Betae ◽  
Mechanical Inoculation ◽  
Production Region ◽  
Das Elisa

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.

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