Fig. 4. Effect of genetic inactivation of p110 or p110 on chemotaxis of BMMs. (A) Chemotaxis of BMMs exposed to a gradient of CSF1 in Dunn chambers, monitored for 16 hours by time-lapse microscopy. The cell tracks from three separate experiments were merged into a single file for analysis. Circular histograms (upper panels) show the proportion of cells migrating into each of 20 segments of the angular trajectory plot (measured when each cell migrated past a horizon of 30 µm from its starting point with the source of CSF1 at the top). Arrows indicate significant mean directionality of the cell population. The green shaded areas mark the 95% confidence intervals of statistical significance. Similar chemotaxis plots were obtained for horizon limits of 50, 80, 100 µm, although the cell numbers varied (not shown). Vector plots (lower panel) show the end point of the cells with the starting point of each cell at the intersection between x and y axes and with the source of CSF1 at the top of each plot. (B) Summary of the effect of genetic inactivation of p110 or p110 on the activation of Rac1 and RhoA, and on chemotaxis. (C) Effect of pharmacological inactivation of PI3K isoforms on chemotaxis in BMMs and BAC1.2F5 cells. Cells on the lower surface of the top chamber were stained and counted from at least six randomly chosen frames. ^*P<0.05 compared with DMSO-treated cells.