The vaccinia virus F11L gene product facilitates cell detachment and promotes migration.

We previously showed that infection with vaccinia virus (VV) induces cell motility, characterized by contractility and directed migration. Motility is temporally regulated because cells are motile immediately after infection, whereas late in infection motility ceases and cells resettle. Motility and its cessation are accompanied by temporal rearrangements of both the microtubule and the actin networks. Because the F11L gene has previously been implicated in VV-induced migration, we now explore the role of F11L in contractility, migration, the cessation of motility and the cytoskeletal rearrangements. By live cell imaging using a VV that lacks an intact F11L gene, we show that F11L facilitates cell detachment and is required for migration but not for contractility. By light microscopy, F11L expression induces a remodeling of the actin, but not the microtubule, network. The lack of migration correlates with smaller plaques, indicating that this process facilitates cell-to-cell spreading of VV. Late in infection, when motility ceases, cells re-establish cell-to-cell contacts in an F11L-independent manner. We finally show that VV-induced motility and its cessation correlate with a temporal regulation of the guanosine triphosphatase RhoA as well as the expression levels of F11L during the infectious cycle.