Skip to main content
. 2011 Sep 13;30(22):4523–4538. doi: 10.1038/emboj.2011.326

Figure 3.

Figure 3

Both WD/E motifs contribute to KLC1/2 recruitment and viral spread. (A) Histograms and scatter plot showing the distribution of the speeds and run lengths of virus moving towards the cell periphery in cells infected with A36–YdF–YFP (black) as well as WE/AA (green) and WD/AA (red) viruses for 8 h. Inserts show the average values for both parameters and error bars represent s.e.m. for 65 virus particles in four independent experiments. (B) Immunofluorescence images showing RFP–KLC2 is not associated with the WD or WEWD viruses (yellow arrows) after they have fused with the plasma membrane at the cell periphery at 11 h post-infection. Pink arrows highlight association of RFP–KLC2 with DAPI-positive WT and WE viruses. Scale bar=10 μm. (C) Analysis of GST pull-down experiments showing the effect of mutating WD/WE motifs on the ability of the cytoplasmic domain of A36 to interact with HA–KLC1 (left panel), HA–KLC2 (middle panel) or endogenous kinesin-1 detected with anti-Kif5B antibody (right panel). Mutation of the WD motif weakens the association of A36 with KLC1/2 and kinesin-1, while mutation of both motifs abrogates all binding.