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. 2018 Nov 19;9:4859. doi: 10.1038/s41467-018-07253-3

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Loss of α-Klotho drives mitochondrial dysfunction and disrupts mitochondrial DNA integrity. a TEM images of young, old, young + scramble and young + siRNA MPCs showing mitochondria (M), lipid droplet accumulation (L), as well as endoplasmic reticuli (ER). Scale: 400 nm. b, c Seahorse analysis of young, old, young + scramble and young + siRNA MPCs quantifying the basal oxygen consumption rate (OCR). d Seahorse analysis of basal OCR of MPCs isolated from wild-type and Kl^+/− mice. e, f Seahorse analysis of reserve capacity (calculated as the difference between basal and maximum OCR) of young, old, young + scramble and young + siRNA MPCs. g Seahorse analysis of reserve capacity of MPCs isolated from wild-type and Kl^+/− mice. h, i RT-qPCR based analysis of mtDNA damage in young, old, young + scramble and young + siRNA MPCs. j RT-qPCR analysis of mtDNA damage in MPCs isolated from wild-type and Kl^+/− mice (*p < 0.05, **p < 0.01, ****p < 0.0001, one-tailed Student’s t test). Data represented as mean ± SEM