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. 2016 Oct 13;5:e19749. doi: 10.7554/eLife.19749

Figure 3. NMN deamidase does not protect axons by reducing NMN levels or by elevating NaMN or NaAD.

Figure 3.

(a, b) Metabolites were analyzed from control or NMN deamidase (NMN DD)-expressing neurons. Nicotinic acid mononucleotide (NaMN) and nicotinic acid adenine dinucleotide (NaAD) levels were normalized to those present in NMN DD-expressing neurons. NMN and NAD+ levels were normalized to that of control neurons. Nicotinamide riboside (NR, 5 mM) was added at 24 hr prior to metabolite measurements. Data show the first and third quartile (box height) and median (line in the box) ± 1.5 time interquartile (details in the method), one-way ANOVA (NaMN, F(4, 40) = 71.8, p<2×10–16; NMN, F(4, 40) = 72.69, p=1.64×10–9; NaAD, F(4,40) = 101.3, p < 2×10–16; NAD+, F (4,40) = 121.4, p < 2 x 10–16). *p <1 × 10–10 denotes significant difference from control (for NMN and NAD+) or NMN DD-expressing (for NaMN or NaAD) metabolite levels with Holm- Bonferroni multiple comparison (Figure 3—source data 1, n = 9). (c) Axon degeneration index (DI) of NMN DD and/or NMN synthetase (NMN SN)-expressing neurons from 0 to 72 hr post axotomy; data show the first and third quartile (box height) and median (line in the box) ± 1.5 time interquartile (details in the method). One-way ANOVA (F(24, 200) = 75.06, p<2 × 10–16. *p<0.002, **p<2 × 10–16denote significant difference from control DI before axotomy (Figure 3—source data 1, n = 9).

DOI: http://dx.doi.org/10.7554/eLife.19749.011

Figure 3—source data 1. Steady state cellular NMN, NaMN, NAD+, NaAD levels in control and NMN deamidase expressing neurons with or without NMN synthetase or NMN synthetase + NR (Figure 3a,b).
Axonal degeneration index at 0, 9, 24, 48, 72 hr post axotomy of control and NMN deamidase expressing neurons with or without NMN synthetase or NMN synthetase + NR (Figure 3c).
DOI: http://dx.doi.org/10.7554/eLife.19749.012
elife-19749-fig3-data1.xlsx (17.5KB, xlsx)
DOI: 10.7554/eLife.19749.012