Figure 3. Active Aurora A associates... | Rockefeller University Press

Figure 3.

$Figure 3. Active Aurora A associates with MCAK on MTs. (A–C) Images showing the whole cell (left) and zoomed regions of the leading (green boxes and top right row) and trailing edges (red boxes and bottom right row) of HUVECs at the edge of a monolayer wound expressing Em–Aurora A and either mCherry-MCAK (A), mApple-EB3 (B), or mApple-tubulin (C; see also Video 2). In all panels, the wound edge faces up. (D) Quantification of the fraction of Em–Aurora A that colocalizes with MCAK, EB3, or tubulin under experimental conditions shown in A–C. (E–G) Immunolocalization of pT288–Aurora A and MTs in control (E), Em–Aurora A–expressing (F; inset, Em–Aurora A localization), and wound-edge HUVECs treated with an Aurora A inhibitor (G). Bars: (main) 10 µm; (zoomed) 2 µm; (F, inset) 10 µm. *, P < 0.05. Error bars show ± standard deviation.$

Active Aurora A associates with MCAK on MTs. (A–C) Images showing the whole cell (left) and zoomed regions of the leading (green boxes and top right row) and trailing edges (red boxes and bottom right row) of HUVECs at the edge of a monolayer wound expressing Em–Aurora A and either mCherry-MCAK (A), mApple-EB3 (B), or mApple-tubulin (C; see also Video 2). In all panels, the wound edge faces up. (D) Quantification of the fraction of Em–Aurora A that colocalizes with MCAK, EB3, or tubulin under experimental conditions shown in A–C. (E–G) Immunolocalization of pT288–Aurora A and MTs in control (E), Em–Aurora A–expressing (F; inset, Em–Aurora A localization), and wound-edge HUVECs treated with an Aurora A inhibitor (G). Bars: (main) 10 µm; (zoomed) 2 µm; (F, inset) 10 µm. *, P < 0.05. Error bars show ± standard deviation.