STAT3 is a pace keeper of adhesion dynamics in migrating astrocytes. (A) Ablation of STAT3 in astrocytes does not result in the destabilization of the microtubule cytoskeleton. Quantitative analysis even shows a moderate increase of α-tubulin IR in STAT3-CKO astrocytes (unpaired t test, n = 221 and 241 WT and STAT3-CKO astrocytes, respectively). Bars, 10 µm. (B) The polarization of STAT3-CKO astrocytes in response to a wound scratch is not significantly affected. Green, β-COP; blue, nuclear staining by Hoechst. Bars, 20 µm. MTOC, microtubule organizing center. (C) The protrusions formed 16 h after wounding are shorter in STAT3-CKO astrocytes (n = 324 WT and 225 STAT3-CKO cells, three independent experiments, Mann-Whitney U test). Bar, 20 µm. (D) STAT3-CKO astrocytes seeded onto laminin exhibit longer FAs than WT cells. Bars, 10 µm. We analyzed 175 and 279 FAs, respectively, from seven WT and eight STAT3-CKO astrocytes. (Mann-Whitney U test). (E) The effect of FAK inhibitor (PF573228; 0, 1, and 3 µM from left to right) on the migration of WT and STAT3-CKO astrocytes. (F) Phosphorylation levels of FAK on Y576 and Y397 exclude defective activation of FAK in STAT3-CKO cells. (G) Control of astrocyte migration by STAT3 does not involve modulation of adhesion strength. (H) Time-lapse analysis of migrating astrocytes transfected with RFP-CrkI revealed that STAT3 is necessary for the timely coordination of FA dynamics with forward cell locomotion (Video 1). Bars, 10 µm. (I) Quantitative analysis confirmed an extended FA lifetime in STAT3-CKO cells (n = 89 and 130 FAs analyzed in 13 WT and 13 STAT3-CKO astrocytes, respectively; Mann-Whitney U test). ns, not significant. Error bars indicate ±SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001.