Fig. 1: Untargeted metabolomics reveals a shared metabolic signature across several senescence models. | Nature Metabolism

Fig. 1: Untargeted metabolomics reveals a shared metabolic signature across several senescence models.

From: A homoeostatic switch causing glycerol-3-phosphate and phosphoethanolamine accumulation triggers senescence by rewiring lipid metabolism

Fig. 1

a, Experimental design for the integrative analysis of time-resolved metabolome and transcriptome datasets obtained from WI38 fibroblasts undergoing RAS and RAF OIS, etoposide-mediated DDIS, RS and quiescence (Q). D, day. b–e, Heat maps showing modules of temporally coexpressed metabolites in WI38 fibroblasts for the indicated senescence inducers at indicated time points using a hierarchical clustering method (WGCNA). Roman numerals refer to different metabolite modules. Data are expressed as row z scores collected from three biologically independent experiments per condition. GSSG, glutathione disulfide (oxidized glutathione); UDP-Gal/Glc, uridine diphosphate galactose/glucose; UDP-GlcNAc, uridine diphosphate N-acetylglucosamine. f, Integrated dynamic metabolome PCA for cells undergoing RAS and RAF OIS, DDIS, RS and Q as control. Metabolite levels were normalized by the ComBat tool. Dashed lines depict the metabolome trajectory for each treatment. g, Correlation circle for the percentage contribution of the indicated metabolites to principal components PC1 and PC2 of f.

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