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Fig. 4. Tctp deficiency impairs axon extension in vivo. (A) Schematic of the experiment. con-MO-injected or tctp-MO-injected stage 28 embryos were electroporated with gap-RFP to label retinal axons and allowed to develop until stage 40 before in vivo brain imaging. (B,C) Representative time-lapse images of gap-RFP-labelled control (top) and Tctp-depleted (bottom) RGC axons coursing through the optic tract. Dotted lines approximate the boundary of the optic tectum. (D) Average extension rates measured from time-lapse recordings of RGC axons coursing through the ventral optic tract (VOT) and dorsal optic tract (DOT) in controls and Tctp morphants. VOT, ***P<0.0001; DOT, *P<0.0273. (E) Percentage of axons with stalled progression in the control and morphant backgrounds. **P<0.0035. (F) Retinotectal projection angular spreads in controls and Tctp morphants. Pre-turn, **P<0.0082; post-turn, ***P<0.0001. (D-F) Mean±s.e.m.; n, number of axons (D) or embryos (E,F) analysed; unpaired t-test. Scale bars: 25 μm. Image published in: Roque CG et al. (2016) © 2016. This image is reproduced with permission of the journal and the copyright holder. This is an open-access article distributed under the terms of the Creative Commons Attribution license Larger Image Printer Friendly View

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