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. 2018 Mar 29;8:5368. doi: 10.1038/s41598-018-23690-y

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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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Nuclear DNA-damage does not relocate EXD2 to the nucleus. (panel a) HeLa cells were treated with 13 Gy X-irradiation to induce nuclear DNA damage and allowed to recover for 30 minutes. Results show that H2AX phosphorylation is considerably increased in the nucleus following this damage whereas EXD2 retains its predominant mitochondrial localization similar to its location in control cells. (panel b) U2OS cells were treated with 250 µg/ml Zeocin for 1 hr and allowed to recover for 1 hr after replacing the Zeocin-containing medium with regular medium. Cells were then processed for IF detection of γH2AX and EXD2 and show a similar result as the X-irradiation in HeLa cells.