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. 2016 Aug 23;113(36):10091–10096. doi: 10.1073/pnas.1604720113

Fig. 1.

Fig. 1.

PLEKHG3 localizes to the leading edge of the cell and controls cell migration. (A) The localization of nine GEFs at the PM, microtubules, and actin filaments in NIH 3T3 cells. (See Fig. S1 and Table S1.) (B) Cells overexpressing seven of the nine GEFs showed increases in the average velocity of cell migration in the FBS-containing medium compared with the control-expressing cells of these GEFs (n > 250). (C) Changes in cell morphology and the localization of CFP-C1 and CFP-PLEKHG3 during cell migration. (See Fig. S2 and Movie S1.) (D) A schematic for the generation of knockout (KO) hESC lines using the CRISPR/Cas9 system. (E) The endogenous PLEKHG3 localization of H9 and PLEKHG3−/− cells. PLEKHG3 is located at the leading edge of migrating cells in H9 cells but not in PLEKHG3−/− cells. The length (yellow line) is the longest distance between any two points along the boundary; the width (blue line) is the secondary axis of the best fit ellipse of the cells. (F) Quantification of the length/width ratio of H9 and PLEKHG3−/− cells: PLEKHG3−/− cells showed a longer morphology than the control cells (n >100). (G) The average velocity of cell migration decreased in PLEKHG3−/− cells (n > 150). (See Figs. S3–S5.) The data represent mean ± SEM; *P < 0.1; **P < 0.01. (Scale bars, 20 μm.)