scholarly journals Occurrence of resistance-breaking strains ofBeet necrotic yellow vein virusin sugar beet in northwestern Europe and identification of a new variant of the viral pathogenicity factor P25

2014 ◽  
Vol 64 (1) ◽  
pp. 25-34 ◽  
Author(s):  
K. Bornemann ◽  
B. Hanse ◽  
M. Varrelmann ◽  
M. Stevens
Keyword(s):  
Sugar Beet ◽  
Yellow Vein ◽  
Pathogenicity Factor ◽  
Resistance Breaking ◽  
New Variant

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 The P25 Pathogenicity Factor of Beet necrotic yellow vein virus Targets the Sugar Beet 26S Proteasome Involved in the Induction of a Hypersensitive Resistance Response via Interaction with an F-box Protein

2012 ◽  
Vol 25 (8) ◽  
pp. 1058-1072 ◽  
Author(s):  
Heike Thiel ◽  
Kamal Hleibieh ◽  
David Gilmer ◽  
Mark Varrelmann
Keyword(s):  
Sugar Beet ◽  
26S Proteasome ◽  
Yellow Vein ◽  
In Planta ◽  
Hypersensitive Resistance ◽  
Resistance Response ◽  
Scf Complex ◽  
Pathogenicity Factor ◽  
F Box Protein

P25, a Beet necrotic yellow vein virus (BNYVV) pathogenicity factor, interacts with a sugar beet protein with high homology to Arabidopsis thaliana kelch repeat containing F-box family proteins (FBK) of unknown function in yeast. FBK are members of the Skp1-Cullin-F-box (SCF) complex that mediate protein degradation. Here, we confirm this sugar beet FBK–P25 interaction in vivo and in vitro and provide evidence for in planta interaction and similar subcellular distribution in Nicotiana tabacum leaf cells. P25 even interacts with an FBK from A. thaliana, a BNYVV nonhost. FBK functional classification was possible by demonstrating the interaction with A. thaliana orthologs of Skp1-like (ASK) genes, a member of the SCF E3 ligase. By means of a yeast two-hybrid bridging assay, a direct effect of P25 on SCF-complex formation involving ASK1 protein was demonstrated. FBK transient Agrobacterium tumefaciens–mediated expression in N. benthamiana leaves induced a hypersensitive response. The full-length F-box protein consists of one F-box domain followed by two kelch repeats, which alone were unable to interact with P25 in yeast and did not lead to cell-death induction. The results support the idea that P25 is involved in virus pathogenicity in sugar beet and suggest suppression of resistance response.

scholarly journals Analysis of the Resistance-Breaking Ability of Different Beet necrotic yellow vein virus Isolates Loaded into a Single Polymyxa betae Population in Soil

2011 ◽  
Vol 101 (6) ◽  
pp. 718-724 ◽  
Author(s):  
Kathrin Bornemann ◽  
Mark Varrelmann
Keyword(s):  
Sugar Beet ◽  
Point Mutations ◽  
The United States ◽  
Yellow Vein ◽  
Polymyxa Betae ◽  
Type Isolate ◽  
Pathogenicity Factor ◽  
Vector Population ◽  
P Type ◽  
Virus Isolates

The genome of most Beet necrotic yellow vein virus (BNYVV) isolates is comprised of four RNAs. The ability of certain isolates to overcome Rz1-mediated resistance in sugar beet grown in the United States and Europe is associated with point mutations in the pathogenicity factor P25. When the virus is inoculated mechanically into sugar beet roots at high density, the ability depends on an alanine to valine substitution at P25 position 67. Increased aggressiveness is shown by BNYVV P type isolates, which carry an additional RNA species that encodes a second pathogenicity factor, P26. Direct comparison of aggressive isolates transmitted by the vector, Polymyxa betae, has been impossible due to varying population densities of the vector and other soilborne pathogens that interfere with BNYVV infection. Mechanical root inoculation and subsequent cultivation in soil that carried a virus-free P. betae population was used to load P. betae with three BNYVV isolates: a European A type isolate, an American A type isolate, and a P type isolate. Resistance tests demonstrated that changes in viral aggressiveness towards Rz1 cultivars were independent of the vector population. This method can be applied to the study of the synergism of BNYVV with other P. betae-transmitted viruses.

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.

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