The cauliflower mosaic virus (CaMV) transmission body response: attempts to unravel a mystery

BGPI : équipe 2National audienceTo move between hosts, many plant viruses such as the Cauliflower mosaic virus (CaMV) use aphids as vectors. When the insects feed on infected leaves, virus particles already present in the leaf attach to their mouth parts (stylets). This enables the viruses to be transferred to a new host plant. As a prerequisite for CaMV transmission, the viral helper protein P2 acts as a molecular linker and mediates binding of the virus particles to the aphid stylets. P2 is available in infected plant cells in a specific structure that is formed beforehand during CaMV infection. This structure is specialized for transmission and named the transmission body (TB). When inserting its stylets into an infected leaf the aphid triggers ultra-rapid explosion of the TB. As a consequence, P2 is redistributed onto cortical microtubules, together with viral particles (that are simultaneously set free from intracellular storage sites) and forms the so- called mixed networks (MNs). The MNs are the predominant viral form that is acquired by aphids; inhibiting their formation reduces drastically transmission rates. Even though the importance of P2MNs for transmission is well established, the P2 motifs and domains involved in formation and functionality of the TB are mostly unknown. We used “Alanine scanning” (as a tool) to generate a set of P2 mutants. These were analyzed for their capacity to form TBs and induce MNs in infected cells, for interaction with microtubules, and for transmission activity in membrane feeding assays. The results allow to define distinct P2 regions that are presented.In another project, we want to identify elicitors that trigger the TB response. For this, we screen different compounds for their capacity to induce MNs in CaMV-infected protoplasts. Preliminary results conferred a role to chitin. In parallel, an Arabidopsis thaliana mutant screen has been initiated as a way to dissect the genetic and molecular basis of signal perception and signal transduction pathways involved in the TB response. The latest results will be presented