Fig. 2: Differential requirement of glycolysis and oxidative metabolism for axon growth and branching. | Nature Communications

Fig. 2: Differential requirement of glycolysis and oxidative metabolism for axon growth and branching.

From: The AMPK-related kinase NUAK1 controls cortical axons branching by locally modulating mitochondrial metabolic functions

Fig. 2

A Main pathways of glucose metabolism. Galactose was used to negate the metabolic effect of glycolysis. Pyruvate was used to support mitochondrial metabolism in a glucose-free medium. Low doses of rotenone were used to lower mitochondrial Complex I activity. Created with BioRender.com. B Representative images of mVenus-expressing cortical neurons (5DIV) cultured in neurobasal medium with the indicated concentrations of glucose. Red stars: collateral branches. C–I Quantification of axon length and collateral branches of 5DIV neurons in the indicated conditions: C, D medium containing increasing concentrations of glucose or pyruvate (PYR). F, G 25 mM glucose-containing medium with increasing doses of rotenone. H, I medium containing either glucose (25 mM, i.e., GLC), galactose (24 mM) + glucose (1 mM, i.e., GAL), or pyruvate (10 mM) without glucose (i.e., PYR). Data: box-and-whisker plots. The horizontal line inside the box is the median value. The endpoints of the box represent the 25th−75th percentiles, with whiskers at minimum and maximum values. Statistical test: Kruskal-Wallis test with Dunn’s post-test (each condition compared to untreated 25 mM condition). C, D N(0mM)= 48, N(0mM+Pyr)= 75, N(2.5mM)= 244, N(5mM)= 191, N(25mM)= 238. E, F N(0nM)= 120, N(10nM)= 102, N(20nM)= 82, N(50nM)= 44. G, H N(Glucose)= 246, N(Galactose)= 248, N(Pyruvate)= 130. ns not significant, *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001. Source data are provided as a Source Data file.

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