Skip to main content
. 2009 May 22;5(5):e1000442. doi: 10.1371/journal.ppat.1000442

Figure 5. Cytoplasmic dynein and kinesin-1 drive axonal CAV-2 transport in MNs.

Figure 5

MNs were incubated for 45 minutes with CAV-Cy3, fixed and stained for molecular motor components. (A) Dynein heavy chain (DHC) colocalises with CAV-2 in MN axons (arrowheads show double-positive structures). Quantification is shown on the right (3 independent experiments, 168 virions in total; error bars represent 5.2%). (B) Kinesin heavy chain (KHC) is associated with a subpopulation of CAV-2 (arrowheads). Quantification of 3 independent experiments is shown on the right (83 virions in total; error bars represent 1.14%). (C–F) MNs were microinjected with either GFP or GFP-p50 or GFP-TPR expression plasmids and imaged live after CAV-Cy3 infection. Representative kymographs show a strong inhibition of CAV-2 transport in either GFP-p50-expressing (C) or GFP-TPR-expressing (D) MNs. An example of a CAV-2 carrier resuming bidirectional transport after a pause is highlighted in red, whilst stopped virions are in green. (E) Kymograph of a GFP expressing neuron showing normal CAV-2 transport. (F) Quantification of the effect of inhibiting cytoplasmic dynein and kinesin 1 on CAV-2 axonal transport. A minimum of 3 independent experiments was performed for each condition; 112 (GFP), 54 (p50) and 52 (TRP) virions in total. Scale bars: (A) 5 µm; (B) 10 µm.