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. Author manuscript; available in PMC: 2021 Oct 6.
Published in final edited form as: Neurobiol Dis. 2019 Nov 15;134:104678. doi: 10.1016/j.nbd.2019.104678

Fig. 3. NMNAT2 depletion reflects impairment of both axonal transport and synthesis.

Fig. 3

(A) Representative immunoblot of wild-type SCG cell bodies/ganglia extracts probed for NMNAT2 and β-actin (loading control) at the indicated time points after CCCP treatment. (B) Quantification of normalised NMNAT2 levels (to β-actin) is shown, with data presented relative to DMSO control (Mean ± SEM; n = 4; oneway ANOVA followed by Bonferroni post-hoc test; ****, p < 0.0001; **, p < 0.01; *, p < 0.05). (C) Representative kymographs of wild-type SCG dissociated cultures expressing NMNAT2-EGFP. (D) Quantification of the % of motile NMNAT2 at the indicated time points after CCCP treatment from 3 neurites per condition in 4 independent experiments (Mean ± SEM; n = 4; two-way ANOVA followed by Sidak post-hoc test; *, p < 0.05. NS, non-significant). (E) Quantification of the % of motile bidirectional, anterograde and retrograde NMNAT2 at the indicated time points after CCCP treatment from 3 neurites per condition in 4 independent experiments (Mean ± SEM; n = 4; two-way ANOVA followed by Sidak post-hoc test; NS, non-significant).