Tobacco mosaic virus movement protein enhances the spread of RNA silencing

Eukaryotic cells restrain the activity of foreign genetic elements, including viruses, through RNA silencing. Although virusesencode suppressors of silencing to support their propagation, viruses may also exploit silencing to regulate host geneexpression or to control the level of their accumulation and thus to reduce damage to the host. RNA silencing in plantspropagates from cell to cell and systemically via a sequence-specific signal. Since the signal spreads between cells throughplasmodesmata like the viruses themselves, virus-encoded plasmodesmata-manipulating movement proteins (MP) mayhave a central role in compatible virus:host interactions by suppressing or enhancing the spread of the signal. Here, we haveaddressed the propagation of GFP silencing in the presence and absence of MP and MP mutants. We show that the proteinenhances the spread of silencing. Small RNA analysis indicates that MP does not enhance the silencing pathway but ratherenhances the transport of the signal through plasmodesmata. The ability to enhance the spread of silencing is maintainedby certain MP mutants that can move between cells but which have defects in subcellular localization and do not supportthe spread of viral RNA. Using MP expressing and non-expressing virus mutants with a disabled silencing suppressingfunction, we provide evidence indicating that viral MP contributes to anti-viral silencing during infection. Our resultssuggest a role of MP in controlling virus propagation in the infected host by supporting the spread of silencing signal. Thisactivity of MP involves only a subset of its properties implicated in the spread of viral RNA.