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. 2018 Jul 9;8:10344. doi: 10.1038/s41598-018-28690-6

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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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Topo IIβ is recruited to laser-damaged sites. (A) Recruitment of Topo IIβ to damaged sites. DNA damage was induced by pulsed UVA laser microirradiation of the nucleus of HeLa cells. After 10 min incubation at 37 °C, the cells were fixed and subjected to coimmunostaining for Topo IIβ and phosphorylated serine 2056 (pS2056) of DNA-PKcs. (B) Tight association of Topo IIβ with damaged chromatin. DNA damage was induced by pulsed UVA laser microirradiation. (Upper) The cells were fixed and coimmunostained for Ku70 and Topo IIβ. (Lower) The cells were treated with CSK buffer containing 0.5% Triton X-100 and subsequently subjected to fixation followed by immunostaining for Topo IIβ and Ku70.