Lipidomic profiling of PEX11β knockout T-REx 293 cells reveals lipid shifts suggesting potential metabolic perturbations

Figures

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  Fig. 1. PEX KO cells demonstrate divergent LC-MS lipid profiles. (a) Principal component analysis (PCA) in positive ion mode shows complete lipidomic separation among all cell lines (n = 7 for WT; n = 3 for all others). (b) Volcano plots highlight differences in PEX KO cells from the WT. PEX3 and PEX14 KO cells are lower in ether (blue) and plasmalogen (green) phosphatidylcholines (PCs) and higher in very-long-chain fatty acid-containing lipids (red). PEX11β KO cells are similar to the WT but differ most in two ceramide species (lower right).

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  Fig. 2. Heatmap of lipid analytes in T-REx293 WT and PEX KO cell samples. Relative abundances of lipid analytes (log10(fold change), normalized to the average of all samples). Lipid annotations are shown to the right of the heatmap. PEX11β KO (n = 3 biological replicates) and WT (n = 7) cells have similar lipid profiles apart from highly enriched analytes in PEX11β KO (CerPE(34:1, O2) through PE(16:0_16:1)). The PEX3 KO (n = 3) profile differs most from the WT. The lipid profile of PEX14 KO (n = 3) represents an intermediate between PEX3 KO and WT.

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  Fig. 3. Effect of G6PDi-1 on T-REx293 WT and PEX KO cell viability. T-REx 293 cell lines were treated 72 h (n = 3 biological replicates, in two separate batches) with G6PDi-1. PEX3 KO cells (a) have increased resistance (p < 0.0001 compared to WT and PEX14 KO) to G6PDi-1-mediated NADPH depletion, while PEX14 KO cells did not differ significantly (p = 0.6332) from WT cells. PEX11β KO cells (b) showed increased sensitivity to G6PDi-1 (p < 0.0001).