Fig. 2: ATP synthase deficiency leads to increased consumption of pantothenate. | Communications Biology

Fig. 2: ATP synthase deficiency leads to increased consumption of pantothenate.

From: Metabolic costs and trade-offs of hypermetabolism in human motor neurons with ATP synthase deficiency

Fig. 2

A Scheme depicting the metabolic tracing experimental plan. On day 30 of the MN differentiation, the media was replaced with media-containing U13C-glucose. Intracellular metabolites were extracted 1, 12 or 48 h later. Six individual wells per cell line were used as replicates. B Cartoon showing the expected fate of the labeled carbons derived from U13C-Glucose. C Volcano plot showing significant changes in metabolites 48 h, comparing pooled mutant samples (52% and 54% mutants, MUT) versus wild-type (samples (0%(1) and 0%(2), WT). Thresholds: FDR = 0.05, log2(FC) = 1. Only relevant metabolites were labeled. Relative abundance of representative glycolysis (D) and OxPhos (E) metabolites after 48 h of isotopic labeling, calculated as the total sum of the labeled fraction (m + 1 to m + n) and referred to one control group 0%(1). F Relative abundance of pantothenate after 48 h of isotopic labeling. Pantothenate cannot be synthetized within the cell, and therefore is not labeled (m + 0). Data shown as mean ± standard deviation, *p < 0.05, **p < 0.01, ***p < 0.001, # vs all, by One-Way ANOVA followed by Tukey´s multiple comparison post-hoc test.

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