Fig. 1From: The microtubule plus-end-tracking protein TACC3 promotes persistent axon outgrowth and mediates responses to axon guidance signals during developmentTACC3 promotes axon outgrowth velocity and prevents spontaneous axon retractions. a, Axon outgrowth velocity is significantly decreased in TACC3-depleted axons by 27% (n = 56) and in TACC3 OE, to a lesser extent, by 11% (n = 106) compared to control (GFP only) conditions (n = 58). b, Retraction rate increased 5 fold in TACC3 KD (n = 107) and decreased 0.6 fold in TACC3 OE (n = 155) in comparison to their corresponding non injected (n = 95) and GFP injected (n = 180) controls respectively. c, d, MT growth velocity (DMSO, n = 9, KHS-101, n = 9) (c) and axon outgrowth length (DMSO, n = 8, KHS-101, n = 12) (d) are significantly reduced by 28 and 26% respectively after acute depletion of TACC3 by the inhibitor KHS101. e, Schematic representation of GFP-tagged TACC3 full-length and deletion constructs, along with plus-end tracking ability (denoted by “+”) and impact on axon outgrowth length. f, Quantification of axon outgrowth length in cultured neural explants of GFP injected control (n = 997), full-length GFP-TACC3 (1-931aa) (n = 787), GFP-TACC3-ΔN (133–931) (n = 613), GFP-TACC3- ΔΔN (363–931) (n = 563) and GFP-ΔTACC domain (1-635aa) (n = 764). *p < 0.05, **p < 0.01, ***p < 0.001. ns not significant. n = axon/growth cone numberBack to article page