Effects of Soil Properties on the Occurrence of Beet Necrotic Yellow Vein Virus and Beet Soilborne Virus on Sugar Beet in Tokat, Turkey

2004 ◽  
Vol 3 (2) ◽  
pp. 56-60 ◽  
Author(s):  
Nazli Dide Kutlu ◽  
Yusuf Yanar . ◽  
Hikmet Gunal . ◽  
Semih Erkan .
Pedosphere ◽  
2021 ◽  
Vol 31 (4) ◽  
pp. 572-582
Author(s):  
Barbara Samartini Queiroz ALVES ◽  
Katherin Prissila Sevilla ZELAYA ◽  
Fernando COLEN ◽  
Ledivan Almeida FRAZÃO ◽  
Alfredo NAPOLI ◽  
...  

2009 ◽  
Vol 116 (1) ◽  
pp. 7-9 ◽  
Author(s):  
R. Koenig ◽  
B. Holtschulte ◽  
G. Deml ◽  
P. Lüddecke ◽  
S. Schuhmann ◽  
...  

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.


2020 ◽  
Vol 70 (1) ◽  
pp. 219-232 ◽  
Author(s):  
Tetsuo Tamada ◽  
Hirokatsu Uchino ◽  
Toshimi Kusume ◽  
Minako Iketani‐Saito ◽  
Sotaro Chiba ◽  
...  

2001 ◽  
Vol 48 (2) ◽  
pp. 133-150 ◽  
Author(s):  
F Moreno ◽  
F Cabrera ◽  
E Fernández-Boy ◽  
I.F Girón ◽  
J.E Fernández ◽  
...  

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

2009 ◽  
Vol 22 (8) ◽  
pp. 999-1010 ◽  
Author(s):  
Heike Thiel ◽  
Mark Varrelmann

Beet necrotic yellow vein virus (BNYVV) induces the most important disease threatening sugar beet. The growth of partially resistant hybrids carrying monogenic dominant resistance genes stabilize yield but are unable to entirely prevent virus infection and replication. P25 is responsible for symptom development and previous studies have shown that recently occurring resistance-breaking isolates possess increased P25 variability. To better understand the viral pathogenicity factor's interplay with plant proteins and to possibly unravel the molecular basis of sugar beet antivirus resistance, P25 was applied in a yeast two-hybrid screen of a resistant sugar beet cDNA library. This screen identified candidate proteins recognized as orthologues from other plant species which are known to be expressed following pathogen infection and involved in plant defense response. Most of the candidates potentially related to host-pathogen interactions were involved in the ubiquitylation process and plants response to stress, and were part of cell and metabolism components. The interaction of several candidate genes with P25 was confirmed in Nicotiana benthamiana leaf cells by transient agrobacterium-mediated expression applying bimolecular fluorescence complementation assay. The putative functions of several of the candidates identified support previous findings and present first targets for understanding the BNYVV pathogenicity and antivirus resistance mechanism.


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