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. 2015 Aug 3;210(3):401–417. doi: 10.1083/jcb.201506110

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© 2015 Ganguly et al.

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Figure 4. — Axonal F-actin dynamics are dependent on actin turnover. (A and B) Kymographs from an axon transfected with GFP:Utr-CH (to label F-actin) and imaged before/after treatment with 100 nM latrunculin or 100 nM jasplakinolide. (A) Note gradual change in the slopes of the F-actin trails over 15 min of incubation, indicating attenuated polymerization. Drug washout (W/O) restores F-actin dynamics (right). (B) Treatment with jasplakinolide for 10 min essentially eliminates the on/off kinetics, leading to stationary F-actin accumulations along axons. (C) Kymographs of F-actin dynamics before and after treatment with 10 µg/ml nocodazole (NOC; note minimal change; Fig. S3 A). (D–G) Quantification of all F-actin dynamics after pharmacological treatments. Note that in general, actin-modulating drugs (latrunculin [LAT], cytochalasin-D, and jasplakinolide [JASP]) attenuate actin dynamics, whereas the microtubule-disrupting agent nocodazole has no effect. Also note increase in hotspot duration upon cytochalasin-D treatment is likely caused by the actin-capping effect of this agent (Cooper, 1987). Increase in hotspot duration upon jasplakinolide treatment may reflect hyperstabilization of F-actin dynamics. All experiments were performed before and after treating the same axon with the stated drug. For latrunculin treatment, n = 8 axons; cytochalasin-D treatment, n = 8 axons; jasplakinolide treatment, n = 6 axons; and nocodazole treatment, n = 8 axons were imaged. At least three independent repeats were performed for each condition. All values represent means ± SEM; (***, P < 0.001; **, P < 0.01, paired t test). For detailed statistics, see Table S1. Arrows between images represent passage of time in before/after experiments.