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. 2017 Jul 4;27(9):1083–1099. doi: 10.1038/cr.2017.85

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Copyright © 2017 The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Smad5 KO causes deficiency in mitochondrial respiration and malfunction of cellular bioenergetic homeostasis. (A) Electron microscopy images showing mitochondrial morphology in WT, Smad5 KO and pre-rescue hES. Scale bar, 0.5 μm. (B) Oxygen consumption rate (OCR) changes under mitochondrial stress in WT, Smad5 KO and pre-rescue hES as measured using the Seahorse Analyzer (n = 6). (C) Statistics of basal and maximal OCR in B. Data are represented as mean ± SEM of 6 independent experiments. Unpaired two-tailed Student's t-test. ^**P < 0.01. (D) Flow cytometry sorting of hES cells after propidium iodide staining. (E) Statistics of cell viability following serum withdrawal. Data are presented as mean ± SEM in three independent experiments. ^**P < 0.01.