Cell-to-cell movement of Tobacco mosaic virus

AMARI, KHALID; PEÑA, EDUARDO; NIEHL, ANNETTE; KORNER, CAMILLA; HEINLEIN, MANFRED

Bischoffsheim

Workshop; EMBO-workshop Intercellular communication in plant development and disease; 2014

Plant development depends on intercellular communication through plasmodesmata (PD) and involves the cell-to-cell trafficking of macromolecules. Viruses and their movement proteins (MP) use this route to spread infection and, therefore, represent excellent tools to investigate the cellular transport pathways and mechanisms by which informational macromolecules are targeted to PD. Tobacco mosaic virus (TMV) spreads its RNA genome independent of its coat protein, likely through adaptation to cellular mechanisms involved in the assembly and transport of RNA:protein complexes. We previously showed that virus movement is correlated with the ability of the viral MP to form mobile RNA complexes that are formed and transported along the cortical ER-actin network. The complexes move in stop-and-go fashion, whereby the movements pause at cortical sites at which ER-actin network intersects with microtubules (MTs). We propose that these cortical MT-associated ER-sites (c-MERs) represent important hubs of interaction between various membrane? and/or cytoskeleton-dependent transport pathways and that the virus exploits these hubs for the recruitment of host factors required for the development of mobile and anchored VRCs and also for the maturation of the latter into viral factories. Our recent studies indicate that the membrane-associated assembly and transport processes along the ER and at PD involve the activity of specific myosins. The efficiency of a virus to spread through the plant and the outcome of infection with respect to disease also strongly depend on interactions of the virus with the plant defense responses. Here, our work concentrates on the interaction of TMV and related tobamoviruses with the host RNA silencing machinery. Like other viruses, TMV encodes a silencing suppressor that controls the activity of virus- and host-derived small RNAs. In addition, the MP was shown to promote the spread or perception of silencing. Therefore, we aim to determine whether the virus may have evolved strategies to hijack the host RNA silencing machinery and thus to change host gene expression to facilitate spread