Tomato yellow leaf curlvirus (TYLCV) is a monopartite,whitefly-transmitted geminivirus. Previous studies showed that V2 mutants of TYLCV and related viruses tend to induce symptomless infection with attenuated DNA levels, while accumulating close to wild-type (wt) DNA levels in protoplasts. This data, alongside with the fact that no "classical" movement protein has been found for TYLCV had led to recognize V2 as a movement protein.
The discovery of plant silencing mechanisms, followed by the revelation of viral silencing suppressors, V2 included, led us to reconsider the involvement of V2 in viral movement. We conducted a set of experiments employing two mutant versions ofthe virus, one impaired in the silencing suppression activity of V2 and another carrying a non-translatable V2. While both mutant viruses retained the ability to spread in the plant, DNA accumulation levels in the V2 mutants were tenfold lower than those of the wt virus. The low accumulation levels of viral DNA in the mutants were complemented by the silencing suppression of TBSV p19. Thus, the setback in virus proliferation, earlier ascribed to movement impediment, is due to the lack of silencing suppression activity.
Whitefly transmission experiments with the above mutants showed that the silencing suppression activity was dispensable for whitefly transmission, whereas the expression of the complete V2 protein was necessary for transmission of the virus.
In conclusion, we state that V2 has no apparent role in viral spread. Additionally, we reveal a novel, unidentified role for V2 in whitefly transmission.
