du point de vue des lignées non-symptomatiques, il est probable qu'on observe des mutations sur le gène VI, dans la mesure où : « the chlorosis and stunting in P6-transgenic and CaMV-infected plants are dependent on interactions between P6 and components involved in ethylene signalling, and that the suppressor gene product may function to augment these interactions. » Geri et al. 2004. Plant Mol Biol

Broglio, E. P. (1995). “Mutational analysis of cauliflower mosaic virus gene VI: changes in host range, symptoms, and discovery of transactivation-positive, noninfectious mutants.” Mol Plant Microbe Interact 8(5): 755-60. Gene VI of cauliflower mosaic virus (CaMV) has been shown to be a determinant of host specificity of the virus as well as a factor influencing symptom development in infected plants. In addition, it plays a crucial role in viral gene expression through a process of posttranscriptional transactivation. In the present study, linker- insertion mutations within gene VI of a cloned, recombinant cauliflower mosaic virus genome were constructed and tested for infectivity, symptom development on solanaceous plants, and the ability of transactivate viral gene expression. Certain mutations in the first third of the gene resulted in changes in symptoms shown by test plants. Another mutation, also in the first third of the gene, blocked infectivity in the Nicotiana species tested and systemic movement in Datura stramonium. The mutants were also tested in protoplasts for the ability to transactivate virus gene expression. Infectious mutants were invariably positive for transactivation and mutants negative for transactivation were noninfectious. Interestingly, two mutants positive for transactivation were noninfectious, suggesting a second function for gene VI in the infection process. These results further suggest a role for gene VI, as yet not fully understood, in systemic movement of the virus in infected plants.

Pooggin et al. (1998) concluded that mutations occurred within the 35S RNA leader sequence at “a surprisingly low frequency.” The requirement for a functional ribosome shunt could provide one constraint that could limit change within the 35S RNA leader sequence (Shababi et al. 2006).