Figure 7. LKB1 farnesylation and kinase activity coordinate cell motility.

(a) Live-cell imaging of scratch wound assays using HeLa cells stably expressing our panel of GFP-LKB1 plasmids. Representative meandering indices shown for each construct. (b) The meandering index for each cell line was calculated and shown as a bar graph. (c) Area closed for each cell line at 0, 3, and 6 hours post-scratch. (d) The percentage of area closed at 0, 3, and 6 hours was calculated and shown as a bar graph. (e) Model: LKB1 farnesylation promotes its leading edge actin colocalization and signals via RhoA-ROCK to promote stress fiber formation, while LKB1 kinase activity regulates membrane dynamics. Together, LKB1 farnesylation localizes LKB1 to leading edge lamellipodia where LKB1 kinase activity can then regulate nascent adhesion formation and deposition. In part (b), a Kruskall-Wallis test with a p-value of 0.05 showed statistical significance. Significance was then measured between comparisons using Dunn’s multiple comparisons test with a p-value of 0.05. In part (d), wound closure passed the assumptions of parametric tests (homogeneity of variance) and was thus measured using ANOVA followed by Sidak’s multiple comparisons test with a p-value of 0.05. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001. N = 30 cells/condition for meandering; N = 3 scratches/condition for closure. Scale bar: 100 μm. Error bars = SEM.