Immunogold Labeling and Electron Microscopic Screening of Beet Necrotic Yellow Vein Virus in the Fungus Polymyxa betae Infecting Beta vulgaris Root Cortical Parenchyma Cells

1994 ◽  
Vol 155 (5) ◽  
pp. 545-552 ◽  
Author(s):  
F. Dubois ◽  
R. S. Sangwan ◽  
B. S. Sangwan-Norreel
Keyword(s):  
Beta Vulgaris ◽  
Immunogold Labeling ◽  
Yellow Vein ◽  
Polymyxa Betae ◽  
Electron Microscopic ◽  
Cortical Parenchyma ◽  
Parenchyma Cells

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.

scholarly journals Identification of amino acids of the beet necrotic yellow vein virus p25 protein required for induction of the resistance response in leaves of Beta vulgaris plants

2008 ◽  
Vol 89 (5) ◽  
pp. 1314-1323 ◽  
Author(s):  
Soutaro Chiba ◽  
Masaki Miyanishi ◽  
Ida Bagus Andika ◽  
Hideki Kondo ◽  
Tetsuo Tamada
Keyword(s):  
Sugar Beet ◽  
Beta Vulgaris ◽  
Specific Interaction ◽  
Viral Rna ◽  
Yellow Vein ◽  
Single Amino Acid ◽  
Polymyxa Betae ◽  
Resistance Response ◽  
Resistance Phenotype ◽  
Wild Beet

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.

scholarly journals An artificial test substrate for evaluating electron microscopic immunocytochemical labeling reactions.

1987 ◽  
Vol 35 (8) ◽  
pp. 909-916 ◽  
Author(s):  
G D Gagne ◽  
M F Miller
Keyword(s):  
Electron Microscope ◽  
Hepatitis B ◽  
Horseradish Peroxidase ◽  
Polyclonal Antibodies ◽  
Hepatitis B Surface Antigen ◽  
Immunogold Labeling ◽  
Artificial Substrate ◽  
Chemical Fixation ◽  
Electron Microscopic ◽  
Immunocytochemical Studies

We describe an artificial substrate system for optimization of labeling parameters in electron microscope immunocytochemical studies. The system involves use of blocks of glutaraldehyde-polymerized BSA into which a desired antigen is incorporated by a simple soaking procedure. The resulting antigen-impregnated artificial substrate can then be fixed and embedded identically to a piece of tissue. The BSA substrate can also be dried and then sectioned for immunolabeling with or without chemical fixation and without exposing the antigen to dehydrating agents and embedding resins. The effects of various fixation and embedding procedures can thus be evaluated separately. Other parameters affecting immunocytochemical labeling, such as antibody and conjugate concentration, can also be evaluated. We used this system, along with immunogold labeling, to determine quantitatively the optimal fixation and embedding conditions for labeling of hepatitis B surface antigen (HbsAg), human IgG, and horseradish peroxidase. Using unfixed and unembedded HBsAg, we were able to detect antigen concentrations below 20 micrograms/ml. We have shown that it is not possible to label HBsAg within resin-embedded cells using conventional aldehyde fixation protocols and polyclonal antibodies.

Electron microscopic evidence for a neuraminic acid in sow thistle yellow vein virus

Virology ◽  
1972 ◽  
Vol 50 (1) ◽  
pp. 309-311 ◽  
Author(s):  
Peter E. Lee ◽  
Marleen Boerjan ◽  
D. Peters
Keyword(s):  
Neuraminic Acid ◽  
Yellow Vein ◽  
Electron Microscopic ◽  
Microscopic Evidence

Vasopressin decreases immunogold labeling of apical actin in the toad bladder granular cell

1992 ◽  
Vol 263 (4) ◽  
pp. C908-C912 ◽  
Author(s):  
Y. Gao ◽  
N. Franki ◽  
F. Macaluso ◽  
R. M. Hays
Keyword(s):  
Actin Cytoskeleton ◽  
Arginine Vasopressin ◽  
Apical Membrane ◽  
Water Channel ◽  
Granular Cell ◽  
Immunogold Labeling ◽  
Toad Bladder ◽  
Apical Region ◽  
Electron Microscopic ◽  
Relative Extent

Studies with the confocal microscope have shown that arginine vasopressin (AVP) depolymerizes F-actin in the apical region of the toad bladder granular cell. However, the resolution of the fluorescence microscope is not great enough to reveal the exact pattern of depolymerization or the relative extent to which microvillar and subapical membrane actin pools contribute to overall depolymerization. We have developed an electron microscopic immunogold method that shows a significant decrease in immunogold labeling of actin in the region just below the apical membrane, with the decrease most pronounced in regions adjacent to the microvilli. There was no significant change of immunogold labeling within the microvilli themselves. Our studies show a reorganization of the actin cytoskeleton in the region of the granular cell, where water channel-carrying vesicles are positioned and fuse in response to AVP.

Early modifications of the internodal anatomy of Glycine max sprayed with 2,4-DB

1979 ◽  
Vol 57 (12) ◽  
pp. 1340-1344 ◽  
Author(s):  
Thompson Demetrio Pizzolato ◽  
David L. Regehr
Keyword(s):  
Cell Division ◽  
Cell Enlargement ◽  
Secondary Phloem ◽  
Anatomical Changes ◽  
Phloem Parenchyma ◽  
Cortical Parenchyma ◽  
Parenchyma Cells ◽  
Radial Cell ◽  
Orderly Fashion ◽  
Stimulation Of

An aqueous spray of 4-(2,4-dichlorophenoxy)butyric acid (2,4-DB) induces anatomical changes in young Glycine internodes. Four days after spraying, the first symptoms appear outside the cambium when the interfascicular parenchyma cells and the adjacent cortical parenchyma cells enlarge and divide in several planes. Four days later, the metaphloem parenchyma cells in many of the leaf traces undergo considerable periclinal cell division and extensive radial cell enlargement. The phloem parenchyma cells of the late metaphloem and first secondary phloem enlarge and divide in a less orderly fashion. Fifteen days after treatment, the cortical parenchyma is modified into a band of radially seriate cells above the protophloem fibers. Products of this cambium-like region convert the cortex into a callus-like tissue. The size of starch grains is reduced initially in the phloem and xylem and later in the cortex. It appears that the stimuli produced by 2,4-DB move into the internode via the metaphloem of leaf traces. Despite the rapid obliteration of conducting phloem by the 2,4-DB induced stimulation of phloem parenchyma, an accelerated differentiation of secondary phloem compensates for this loss.

Metabolic disturbances in sugar beet (Beta vulgaris) during infection with Beet necrotic yellow vein virus

2020 ◽  
Vol 112 ◽  
pp. 101520
Author(s):  
Kimberly M. Webb ◽  
William M. Wintermantel ◽  
Lisa Wolfe ◽  
Linxing Yao ◽  
Laura Jenkins Hladky ◽  
...  
Keyword(s):  
Sugar Beet ◽  
Beta Vulgaris ◽  
Yellow Vein ◽  
Metabolic Disturbances
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