Details of DPV and References
DPV NO: 123 July 1973
Species: Oat blue dwarf virus | Acronym: OBDV
Oat blue dwarf virus
E. E. Banttari Department of Plant Pathology, University of Minnesota, St. Paul, Minnesota, USA
R. J. Zeyen Department of Plant Pathology, University of Minnesota, St. Paul, Minnesota, USA
- Main Diseases
- Geographical Distribution
- Host Range and Symptomatology
- Transmission by Vectors
- Transmission through Seed
- Transmission by Grafting
- Transmission by Dodder
- Nucleic Acid Hybridization
- Stability in Sap
- Properties of Particles
- Particle Structure
- Particle Composition
- Properties of Infective Nucleic Acid
- Molecular Structure
- Genome Properties
- Relations with Cells and Tissues
- Ecology and Control
Goto & Moore (1952) and
Blue dwarf virus (Rev. appl. Mycol. 31: 379)
- Flax crinkle virus (Rev. appl. Mycol. 39: 173)
An RNA-containing virus with isometric particles 28-30 nm in diameter. It has a wide experimental host range, is leafhopper-transmitted (multiplies in Macrosteles fascifrons) and is reported from the North American Great Plains from Kansas to Manitoba. It is not sap-transmitted nor seed-borne.
In oats infected early it causes stunting, bluish-green foliage, enations on leaf and stem veins, and sterile florets. Similar symptoms develop in barley but there is less enation formation and bluish-green coloration. Leaf crinkle, stunting and reduced flower-setting are common in flax.
Oat blue dwarf disease is reported from the North American Great Plains from Kansas (Sill, King & Hansing, 1954) to Manitoba (Creelman, 1965). A similar disease is reported from Europe (Raatikainen, 1970; K. Lindsten, pers. comm.).
Host Range and Symptomatology
Hosts are known in 7 families of monocotyledonous and dicotyledonous plants (Banttari & Moore, 1962; Westdal, 1968). Some hosts are infected symptomlessly (Westdal, 1968). Not transmissible by inoculation of sap.
- Avena sativa(common oat). Stunting (Fig. 1), dark bluish-green foliage, enations on veins of leaves and stem (Fig. 2) and sterile florets. Excessive tillering or adventitious culms arising from the nodes above the soil (Banttari & Moore, 1962). Occasional leaf necrosis under field conditions (Heagle & Moore, 1969).
Linum usitatissimum (common flax). Enations along the lateral veins of leaves causing crinkle (Fig. 3, Fig. 4) (Fredericksen & Goth, 1959; Banttari & Fredericksen, 1959).
Stellaria media (common chickweed), Spinacia oleracea (spinach) and Chrysanthemum morifolium (chrysanthemum) all develop leaf enations (Westdal, 1968).
- Cultures have been maintained in Avena sativa, Hordeum vulgare (barley) and Linum usitatissimum. A. sativa, H. vulgare and Spinacia oleracea have been used as sources of virus for purification; A. sativa yields most virus, but only c. 1 mg virus/kg plant tissue.
- There are no known local lesion assay hosts; the most commonly used systemically infected hosts are L. usitatissimum and A. sativa.
A mild variant was noted in the USA but not maintained. A similar disease, whose causal agent is transmitted by Macrosteles laevis, is reported in Europe (K. Lindsten: see Raatikainen, 1970).
Transmission by Vectors
In North America the only known vector is the aster leafhopper, Macrosteles fascifrons. Approximately 25-30% of individuals in natural populations of the leafhopper are capable of transmitting. Transmission is sporadic when individuals are transferred to new assay plants daily. The virus can be acquired within 15 min from infected plants and transmitted to test plants after a 7-day incubation period. Maximum transmission occurs after 14-35 days and individual insects may transmit for more than 2 months (Banttari & Zeyen, 1970). The ability of the vector to transmit is genetically controlled and may be altered by in-breeding (Timian & Alm, 1973).
Leafhoppers become viruliferous after feeding on plant extracts through membranes (Long & Timian, 1971) or after abdominal injection with plant or insect extracts (Banttari & Zeyen, 1969, 1970). The virus multiplies in the insect vector (Banttari & Zeyen, 1972a).
Transmission through Seed
The virus is not seed-transmitted in oats (Banttari & Moore, 1962).
Transmission by Dodder
Transmission reported from flax to flax by Cuscuta sp. (Fredericksen & Goth, 1959).
The virus seems weakly immunogenic; antiserum was obtained with a titre of 1/256 in agar double diffusion plates using purified virus as antigen.
No serological comparisons with other viruses have been made (Banttari, unpublished data).
Stability in Sap
Extracts from infected Hordeum vulgare, ground in 0.01 M phosphate buffer pH 7.0 and membrane-fed to aster leafhoppers, lost infectivity after dilution 1/256-1/512, but retained infectivity after storage for 10 min at 60°C or 16 days at 24°C (Long & Timian, 1972). Extracts from leafhoppers ground in 0.01 M phosphate buffer pH 7.0 were infective when injected into leafhoppers at a dilution of 106 (Banttari & Zeyen, 1972a).
Cellulose column chromatography (Venekamp & Mosch, 1964) followed by sucrose density gradient centrifugation was used to purify the virus (Banttari & Zeyen, 1969). Oat plants were the best source of virus (c. 1 mg virus/kg tissue).
Grind plants in 0.02 M phosphate pH 7.0, 0.008 M MgCl2, squeeze extracts through cheesecloth and centrifuge at 7000 g for 10 min. Retain the supernatant fluid and add polyethylene glycol (Carbowax 6000), NaCl and glucose to 5%, 2%, and 4.5% respectively. Chromatograph in a column of cellulose powder (Whatmans Chromedia CF11) equilibrated with 5% polyethylene glycol, 2% NaCl, 0.004% MgCl2, 4.5% glucose, in 0.01 M phosphate buffer at pH 7.0 until all pigmented and ultraviolet absorbing (260 nm) materials are removed. Elute the virus with 4.5% dextrose, 0.004 M MgCl2 in 0.01 M phosphate buffer, pH 7.0.
Make the virus eluate 5% with respect to NaCl, centrifuge at 65,000 g for 3 hr, resuspend the pellets in buffer (0.01 M phosphate, pH 7.0) and recentrifuge at c. 7000 g for 15 min. Float the supernatant fluid on 10-40% sucrose density gradients (buffered 0.01 M phosphate, pH 7.0) and centrifuge at c. 50,000 g for 2.5 hr. A virus band forms 24-27 mm below the meniscus and may be extracted and concentrated by high speed ultracentrifugation. Store the concentrated virus in 0.01 M phosphate buffer pH 7.0 at 1-4°C or in liquid N2.
Properties of Particles
(Pring, Zeyen & Banttari, 1973; Banttari & Zeyen, 1969).
Sedimentation coefficient: 119 S.
The particles are isometric, 28-30 nm in diameter when mounted in sodium phosphotungstate (Fig. 5). The particles exhibit subunits in the 20-40 Å range when shadow-cast or negatively stained (Zeyen & Banttari, 1972).
RNA: Single-stranded and apparently homogeneous. Sedimentation coefficients, established by linear-log sucrose density gradients, are 31.9 S before formaldehyde treatment and 21.1 S following treatment (Pring et al., 1973). Substitution of the latter value into the formula of Brakke & Van Pelt (1970) gives an estimate of 2.13 x 106 daltons for the M. Wt of the RNA. The RNA is easily liberated from the particles at pH 9.0 in a variety of buffer systems.
Relations with Cells and Tissues
The virus is restricted to phloem tissue and causes hyperplasia and hypertrophy of young phloem and adjacent parenchyma. In Linum usitatissimum there is hyperplasia of phloem-related fibres as well as phloem elements and parenchyma. In Avena sativa the hyperplastic phloem elements are parenchymatous, with truncated end walls. In both flax and oats the virus is found only in phloem elements and is usually enclosed in membrane-bound inclusions.
In oats, crystalline and paracrystalline formations occur (Fig. 6), often large enough to be seen by light microscopy. In plant hosts the virus is not found inside or associated with cell organelles (Banttari & Zeyen, 1971; Zeyen & Banttari, 1972). In plant tissues simultaneously infected with the mycoplasma-like agent of aster yellows, the virus apparently multiplies independently even though both agents are found in the same cells (Banttari & Zeyen, 1972b).
The virus multiplies in leafhoppers; virus particles occur in the neural lamella of the brain and in fat bodies (Banttari & Zeyen, 1972a).
The only other disease of oats that resembles oat blue dwarf disease is oat sterile dwarf, reported in Finland (Ikäheimo, 1961), Czechoslavakia (Prusa, Jermoljev & Vacke, 1959) and Sweden (Lindsten, 1961). Brcák, Kralik & Vacke (1972) reported that cells of plants with this disease contained particles 73 nm in diameter but the particles were not purified or transmitted to prove aetiology. The oat sterile dwarf agent was not transmitted to oats or flax by Macrosteles laevis (E. Banttari & A. Murtomaa, pers. comm., 1965).
(Left) healthy oat, (centre and right) two oat plants infected with oat blue dwarf virus in the first leaf stage; note the stunting and shortening of leaf blades and internodes.
Enations on the major lateral veins of flax leaf, abaxial surface. The depressions on the adaxial surface, combined with enations on the abaxial surface result in the leaf crinkle symptom.
References list for DPV: Oat blue dwarf virus (123)
- Banttari & Fredericksen, Phytopathology 49: 539, 1959.
- Banttari & Moore, Phytopathology 52: 897, 1962.
- Banttari & Zeyen, Phytopathology 59: 183, 1969.
- Banttari & Zeyen, Phytopathology 60: 399, 1970.
- Banttari & Zeyen, Phytopathology 61:1249, 1971.
- Banttari & Zeyen, Phytopathology 62: 745, 1972a.
- Banttari & Zeyen, Virology 49: 305, 1972b.
- Brakke & Van Pelt, Virology 42: 699, 1970.
- Brcák, Kralik & Vacke, Biologia Pl. 14: 302, 1972.
- Creelman, Can. Plant Dis. Surv. 45: 45, 1965.
- Fredericksen & Goth, Phytopathology 49: 538, 1959.
- Goto & Moore, Pl. Dis. Reptr 36: 69, 1952.
- Heagle & Moore, Pl. Dis. Reptr 53: 664, 1969.
- Ikäheimo, Maataloust. Aikakausk. 33: 81, 1961.
- Lindsten, Kungl. LantbrHögsk. Annlr 27: 199, 1961.
- Long & Timian, Phytopathology 61: 1230, 1971.
- Long & Timian, Phytopathology 62: 773, 1972.
- Moore, Phytopathology 42: 471, 1952.
- Pring, Zeyen & Banttari, Phytopathology 63: 393, 1973.
- Prusa, Jermoljev & Vacke, Biologia Pl. 1: 223, 1959.
- Raatikainen, Luonnon Tutk. 75: 65, 1970.
- Sill, King & Hansing, Pl. Dis. Reptr 38: 695, 1954.
- Timian & Alm, Phytopathology 63: 109, 1973.
- Venekamp & Mosch, Neth. J. Pl. Path. 70: 85, 1964.
- Westdal, Can. J. Bot. 46: 1431, 1968.
- Zeyen & Banttari, Can. J. Bot. 50: 2511, 1972.