Jump to Main Content
Contribution of Tomato torrado virus Vp26 coat protein subunit to systemic necrosis induction and virus infectivity in Solanum lycopersicum
- Wieczorek, Przemysław, Wrzesińska, Barbara, Frąckowiak, Patryk, Przybylska, Arnika, Obrępalska-Stęplowska, Aleksandra
- Virology journal 2019 v.16 no.1 pp. 9
- Solanum lycopersicum, Tomato torrado virus, chimerism, coat proteins, elicitors, enzyme activity, genes, leaves, mass spectrometry, messenger RNA, necrosis, pathogenicity, phenotype, plant diseases and disorders, plant response, plant viruses, protein subunits, qualitative analysis, ribonucleases, tomatoes, translation (genetics), viruses
- BACKGROUND: Tomato torrado virus (ToTV) infection manifests with burn-like symptoms on leaves, leaflets and upper stem parts of susceptible infected plants. The symptoms caused by ToTV may be considered as one of the most severe virus-induced forms of systemic necrosis, which spreads within the whole plant and leads to a lethal phenotype. However, to date there are no data revealing which viral genes encode for a specific pathogenicity determinant that triggers the plant necrotic response for any torradovirus. In this study we evaluated the influence of three coat protein subunits of ToTV: Vp23, Vp26 and Vp35, transiently expressed from a PVX-based vector, and checked their association with the induction of systemic necrosis in infected Solanum lycopersicum L. (cv. Beta Lux), a natural host of ToTV. METHODS: To estimate how ToTV coat protein subunits might contribute in plant response to virus infection we over-expressed the proteins from PVX-based vector in tomato and analyzed enzymatic activities related with plant defense response. By doing protein qualitative analysis performed by mass spectrometry we indicated the PR10 in protein fraction with induced ribonuclease activity. RESULTS: We observed that only the Vp26 enhanced PVX pathogenicity causing severe necrosis of the infected plant. Moreover, we indicated increased RNase and oxidative activities in plants infected with PVX-Vp26 chimeras only. Importantly, we suspected that this increased RNase activity is associated with increased accumulation of PR10 mRNA and products of its translation. CONCLUSIONS: On the basis of the obtained results, we indicated that Vp26 acts as the elicitor of hypersensitive response-like reactions of PVX-Vp26 manifesting with enhanced pathogenicity of the recombined PVX. This might be the first described suspected necrosis determinant of torradoviruses infecting tomatoes.