TCV is associated with several dispensable non-coding RNAs known as satellite (sat) RNAs that are dependent on the TCV genomic RNA for replication and propagation. The virulence of TCV infection is affected by the presence of satC (356 bases), a satRNA originally generated by a double recombination event between the avirulent satRNA satD (194 bases) and two regions near the 3' end of TCV genomic RNA. SatC co-infection of turnip enhances the mild stunting and chlorotic symptoms of TCV-infected leaves to severe stunting and crinkling, with an overall dark green coloration. In Arabidopsis thaliana, the stunting and delayed bolting attributed to infection by TCV alone turns into a lethal overall necrosis in the presence of satC, usually within 14 to 21 days postinoculation
TCV symptoms can also be modulated by alterations in its 38 kda coat protein (CP). The TCV CP is involved in a wide variety of functions required for successful host invasion. For example, in addition to TCV symptom modulation, the CP is required for (1) assembly of virions; (2) systemic movement, but not cell-to-cell movement, in Arabidopsis thaliana and Brassica campestris and systemic and cell-to-cell movement in other hosts such as Nicotiana benthamian; (3) elicitation of the salicylic acid-dependent defense response in Arabidopsis ecotype Dijon; (4) repression of satC replication; (4) suppression of an early step in the anti-viral RNA degradation pathway known as RNA silencing ; (5) modulation of satC-associated symptoms. The involvement of the CP in satC symptom modulation was discovered inadvertently when Arabidopsis plants were inoculated with TCV-CPCCFV, in which the TCV CP was replaced with the CP of the related virus Cardamine chlorotic fleck. The mild symptoms expressed by TCV-CPCCFV-infected plants were surprisingly abolished, and virus long-distance movement restricted, in the presence of satC. A similar effect was also found when satC was co-inoculated onto Arabidopsis plants with a mutant of TCV, TCV-CPm, which contained a point mutation in the initiation codon of the CP. This mutant virus produced approximately 10% of wt levels of a CP with two additional amino acids on the N-terminus, with translation initiating at an unstream non-canonical CUG codon. While virions were not detected in plants infected with TCV-CPm, the virus was able to move systemically and produce mild symptoms that were substantially reduced in the presence of satC
We recently found a correlation between wt levels of CP, very low levels of virions, and severe symptoms. Arabidopsis protoplasts inoculated with wt TCV and satC also accumulated substantially reduced levels of virions compared with cells inoculated with TCV. Recent reports indicating that the TCV CP is a suppressor of RNA silencing suggest a model where high levels of free CP found in plants inoculated with either TCV-CPm3 or wt TCV and satC enhance silencing suppression thus promoting movement of TCV. In addition, recent evidence suggesting that virion disassembly may be necessary for viral entry (as an RNA-protein particle) into sieve element cells of the phloem for long-distance transport, suggests that lack of virions assembly may also promote TCV movement and enhancement of pathogenesis.
Publications:
Zhang, F. and Simon, A. E.
(2003)
Enhanced viral pathogenesis associated with a virulent mutant virus
or a virulent satellite RNA correlates with reduced virion accumulation and
abundance of free coat protein. Virology
312, 8-13.
Simon, A.E. (1995) Virus-Arabidopsis Interactions. In: Arabidopsis, E. Meyerowitz and C. Sommerville, eds. Cold Spring Harbor Press, pp 685-704.(Book)
Roux, L., Simon, A.E. and Holland, J.J. (1991) Effects of defective interfering viruses on virus replication and pathogenesis in vitro and in vivo. Advances in Virus Research 40, 181-211.(Book)