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. 2017 Oct 30;7:14348. doi: 10.1038/s41598-017-13905-z

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© The Author(s) 2017

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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DNA damage and repair genes upregulated in Spalax liver as compared to rat. N = 18 genes from the Fanconi Anemia (FA) pathway were transcriptionally upregulated in normoxic Spalax liver, as indicated by the colour chart (prepared using Advaita Bio’s iPathwayGuide; http://www.advaitabio.com/ipathwayguide.html). Note that both, the major activator of this pathway, ATR, and its downstream interacting partner, the helicase WRN are overexpressed on the RNA level in Spalax versus rat liver. The same tendency was shown by RPA, which stimulates the helicase and exonuclease activity of WRN, and by FEN1, which complexes WRN to adjust stalled replication forks.