Fig. 6: Mitochondrial defects trigger conserved transcriptional remodeling. | Communications Biology

Fig. 6: Mitochondrial defects trigger conserved transcriptional remodeling.

From: OxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases

Fig. 6

a t-distributed stochastic neighbor embedding (t-SNE) of RNAseq data from control, SURF1, and Oligo-treated human fibroblasts across the lifespan. b Overlap of significantly upregulated (red) or downregulated (blue) genes in SURF1 and Oligo groups relative to control (linear mixed effects model, FDR-corrected p value < 0.05). Note, outer group counts include shared counts in the overlapping rings. Gray indicates the diverging direction of regulation between SURF1 and Oligo DEGs. c Expression levels of the top 100 differentially expressed genes in SURF1 (<75 days grown) and Oligo-treated cells (days 35–110). d iPAGE analysis of RNAseq data showing the top 40 enriched gene ontology pathways in top overlapping upregulated and downregulated genes, conserved across both SURF1 and Oligo groups relative to control. Note, −log(p value) > 8 are mapped as dark orange. e Gene expression timecourses of select genes related to the ISR, senescence, nucleotide metabolism, and telomere maintenance. Log2 expression values (TPM) are normalized to the median of the control youngest timepoints. n = 3 donors per group, 3–8 timepoints per donor.

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