Fig. 2

Phenotypic and metabolic impact of MIR210 locus deletion. (a) Competitive growth assays of WT and MIR210-KO or MIR210HG-KO clones labeled with GFP or dTomato, analyzed after 3 days of coculture. Flow cytometry results show significantly fewer KO cells compared to WT (mean ± SD from 3 experiments, with four different clones analyzed per experiment; two-way ANOVA, **p < 0.01, ***p < 0.001). (b) Mitochondrial respiration (OCR) in HEK WT and KO clones under basal or stress conditions. Data are mean ± SD from 2 experiments in duplicate (two-way ANOVA, n.s. not significant, ***p < 0.001, ****p < 0.0001). (c) Significant changes in cell cycle distribution in HEK cells (WT and MIR210-KO) under different oxygen levels (two-way ANOVA, *p < 0.05, ****p < 0.0001). (d) OCR profiles from a mito stress test in WT and mir210-KO mouse fibroblasts reveal reduced maximal respiration and spare capacity in KO cells (mean ± SD from a single representative experiment, three replicates). (e) Mitochondrial ROS quantification in WT and mir210-KO mouse fibroblasts after 24-hour exposure using MitoTracker™ Red CM-H2XRos and flow cytometry (mean ± SD from 3 experiments, two-way ANOVA, **p < 0.01). (f) Cell cycle alterations in mir210-KO mouse fibroblasts under different oxygen levels (two-way ANOVA, **p < 0.01). (g) Cellular ultrastructure by transmission electron microscopy shows structural variations in mitochondria and endoplasmic reticulum in KO fibroblasts under hypoxic conditions.