Details of DPV and References

DPV NO: 193 August 1978

Family: Tymoviridae
Genus: Tymovirus
Species: Kennedya yellow mosaic virus | Acronym: KYMV

Kennedya yellow mosaic virus

A. J. Gibbs Research School of Biological Sciences, Australian National University, Canberra, Australia

Contents

Introduction

Described by Dale, Gardiner & Gibbs (1975).

A virus with isometric particles 28 nm in diameter which sediment as two components. Its genome is single-stranded RNA. Readily transmitted by inoculation of sap, infects many species of the Papilionaceae, commonly causing vein yellowing and mottling. Vector not known. Found along the eastern seaboard of Australia.

Main Diseases

Found in nature in several species of the Papilionaceae: Clitoria ternatea, Desmodium scorpiurus, D. triflorum, Indigofera australis and Kennedya rubicunda. Infected plants show a blotchy chlorotic mosaic of the youngest leaves (Fig. 1) and this fades as the leaves mature.

Geographical Distribution

Reported only along the eastern seaboard of Australia from north Queensland to southern New South Wales; not isolated from the few samples obtained from elsewhere in mainland Australia and Tasmania. The three known strains of the virus occur in different localities.

Host Range and Symptomatology

Readily transmitted by inoculation of sap to many species of the Papilionaceae and to two of the Solanaceae, but not to ten other common test plant species (Dale & Gibbs, 1976); plants in 20 out of 34 tribes of papilionate legumes have been tested and 89 of 133 species in 48 of 54 genera found to be susceptible (K. F. Boswell & A. J. Gibbs, unpublished data). Most infected plants show an ephemeral vein yellowing; the plants may become symptomless but tip leaves produced later show a blotchy chlorotic mosaic which fades as the leaves mature.

Diagnostic species

Kennedya rubicunda (red Kennedy pea, dusky coral pea). Systemic vein chlorosis, followed by a persistent blotchy mosaic (Fig. 1).

Phaseolus aureus (mung bean). Necrotic local lesions are produced (Fig. 3), followed by severe chlorotic mottle and necrotic spotting of tip leaves (Fig. 2).

Phaseolus vulgaris (French bean) cvs Redland Pioneer, Pinto, Purple King. Chlorotic local lesions, systemic chlorotic and necrotic mottle.

Pisum sativum (pea). Systemic vein chlorosis.

Datura stramonium and Nicotiana glutinosa. Faint chlorotic local lesions in inoculated leaves only.

Propagation species

Kennedya rubicunda is a good perennial host for maintaining isolates. Vigna sesquipedalis (snake bean) and Pisum sativum (cvs Greenfeast or Early Massey Melbourne Market) are good sources of virus particles for purification.

Assay species

No satisfactory local lesion host is known; P. aureus is perhaps best but very unreliable, and lesion numbers vary greatly depending particularly on the age of the plant when inoculated and also on the weather.

Strains

Three strains have been recognised. These are most readily distinguished by the electrophoretic mobility of their particles (Fig. 4), though they also differ slightly antigenically. The three strains occur in different parts of Australia. All the isolates from within 150 km of Sydney have particles with the electrophoretic mobility of the original Jervis Bay isolate (JB; Fig. 4) and came from K. rubicunda; all isolates from further south in New South Wales have the electrophoretic mobility of the Wapengo isolate (W; Fig. 4) and were from K. rubicunda and Indigofera australis; and all isolates from Queensland have the electrophoretic mobility of the Mount Jukes isolate (MJ; Fig. 4) and came from Clitoria ternatea, Desmodium scorpiurus and D. triflorum. No differences have been found in the host ranges of the three strains among papilionate legumes, though different isolates, even from one locality, often differ in virulence.

Transmission by Vectors

No vector identified. Not transmitted by various species of grasshopper, nor by the phytophagous cockroach Ellipsidion australe. Not transmitted by foliage contact.

Transmission through Seed

Not seed-borne in K. rubicunda, Pisum sativum or Desmodium scorpiurus.

Serology

Particles are strongly immunogenic in rabbits. Antisera with precipitin titres of 1/512 are readily prepared.

Relationships

Belongs to the tymovirus group (Harrison et al., 1971). It is related most closely to clitoria yellow vein virus, both serologically (Koenig, 1976) and in its host range and symptomatology (Bock, Guthrie & Meredith, 1977). It is also closely related to desmodium yellow mottle virus (Walters & Scott, 1972).

Stability in Sap

Stable. In sap from infected P. sativum the dilution end-point is about 10-6, the thermal inactivation point is between 65°C and 70°C, and at about 20°C the sap is infective for 10 days but not 100.

Purification

(Dale & Gibbs, 1976). Homogenize infected P. sativum or Vigna sesquipedalis in 100 mM potassium phosphate, 50 mM ascorbate, pH 7 (2 ml/g leaf). Filter. Clarify by emulsifying with one half volume each of chloroform and n-butanol. Concentrate and purify particles by two cycles of differential centrifugation using 30 mM potassium phosphate, pH 7, for resuspension. Further purify by centrifuging in sucrose density gradients.

Properties of Particles

The particles, like those of other tymoviruses, sediment as two components; a fast sedimenting (B) component of infective nucleoprotein particles, and a slower (T) component of protein shells. The two components are serologically indistinguishable.

Sedimentation coefficients (s20,w): 54 S (T) and 110 S (B).

A260/A280: 0.81 (T), 1.69 (B); unfractionated preparations about 1.63.

Isoelectric point: pH 3.3 (all strains) (M. Fischer, unpublished data).

Particle Structure

Particles are isometric c. 28 nm in diameter (Fig. 5). T particles are penetrated by negative stain and show no structure, most B particles exclude negative stain and show the arrangement of morphological subunits characteristic of tymovirus particles.

Particle Composition

Nucleic acid: RNA, single-stranded, c. 34% of particle weight (estimated from sedimentation data; Reichmann, 1965). M. Wt estimated from particle composition and structure c. 1.9 x 106. Nucleotide composition G 15.2: A 21.9; C 37.4: U 25.4. Isolated RNA is infective. Particles contain no RNA molecules of the size of transfer RNA (J. Cooley, unpublished data), as found in particles of some other tymoviruses (Génevaux, Pinck & Duranton, 1976).

Protein: Single species of M. Wt 20,500 ± 300, estimated by electrophoresis in polyacrylamide gels containing sodium dodecyl sulphate. The particle contains 66% protein by weight. Ala 20 residues, arg 0, asx 14, cys not done, glx 12, gly 9, his 4, ile 15, leu 22, lys 5, met 2, phe 4, pro 17, ser 23, thr 24, trp not done, tyr 6, val 11; total 188, M. Wt 19,500, together with cys and trp probably c. 20,000 (Dale & Gibbs, 1976).

Relations with Cells and Tissues

The chloroplasts in infected cells have marginal vesicles attached to the chloroplast membrane as found with other tymoviruses (Dale et al., 1975).

Notes

The only other virus isolated from K. rubicunda, kennedya virus Y (Dale et al., 1975), is perhaps more widespread than kennedya yellow mosaic virus, from which it is readily distinguished by its filamentous particles, and by the local lesions it produces in C. amaranticolor. Of the tymoviruses, kennedya yellow mosaic virus is most closely related to clitoria yellow vein virus and desmodium yellow mottle virus, but may be distinguished from them serologically and by the electrophoretic mobility of the particles (Koenig, 1976). In addition there are host range differences; for example, kennedya yellow mosaic virus but not desmodium yellow mottle virus infects Glycine max, Nicotiana glutinosa and Datura stramonium, whereas desmodium yellow mottle virus but not kennedya yellow mottle virus infects Trifolium repens, T. incarnatum and Macroptilium atropurpureum.

Figures

References list for DPV: Kennedya yellow mosaic virus (193)

  1. Bock, Guthrie & Meredith, Ann. appl. Biol. 85: 97, 1977.
  2. Dale & Gibbs, Aust. J. biol. Sci. 29: 397, 1976.
  3. Dale, Gardiner & Gibbs, Newsl. Aust. Pl. Path. Soc. 4: 13, 1975.
  4. Génevaux, Pinck & Duranton, Annls. Microbiol. (Inst. Pasteur) 127A: 47, 1976.
  5. Harrison, Finch, Gibbs, Hollings, Shepherd, Valenta & Wetter, Virology 45: 356, 1971.
  6. Koenig, Virology 72: 1, 1976.
  7. Reichmann, Virology 25: 166, 1965.
  8. Walters & Scott, Phytopathology 62: 125, 1972.