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[Preprint]. 2023 Apr 21:2023.02.03.527065. Originally published 2023 Feb 4. [Version 3] doi: 10.1101/2023.02.03.527065

Figure 4. Effect of chronic pharmacological and genetic perturbation of mitochondrial function on Numt accumulation in fibroblasts.

Figure 4.

(A) Time course of Numt accumulation in healthy donors 1–3 and same cells cultured in dexamethasone (Dex) mimicking chronic Dex exposure. (B) Time course of Numt accumulation in healthy donors 1–3 and same cells cultured in oligomycin (Oligo). (C) Numt accumulation time course in the patient fibroblasts with SURF1 gene defect (Patient 1–3) and the ones from three healthy donors (Donor 1–3). (D) Comparision of Slopes derived from all patients untreated, Dex-treated, oligo-treated, and SURF1 gene defect. Numt counts for each group were normalized by the median value. A linear regression analysis was performed to derive the rate of the Numt accumulation and calculate the slopes in each group. ANOVA test was used to test the significance between the slopes of untreated donors and the ones of treated donors or patients in the hypothesis that pharmacological or genetic perturbation would increase the accumulation of Numts. ***, **, and * represent a significant p-value less than 0.001, 0.01, and 0.05, respectively, and ns represents non-significance.