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. 2019 Nov 14;9:16862. doi: 10.1038/s41598-019-53239-6

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© The Author(s) 2019

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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A549 untransfected cells (control), transfected with plasmid His-Dot1L 48 h (His-DOT1L) or treated with pinometostat 48 h (EPZ) were used (A) for immunofluorescence analysis against (His), H3K79me2 and H4K20me2. White arrows denote cells with high expression of His-DOT1L. (B) Western blots against His-DOT1L, H3K79me2, H3 and H4K16ac. (C) Untransfected cells (PR8), transfected with His-Dot1L 48 h (PR8 Dot1L) or treated with pinometostat 48 h (PR8 EPZ), were infected with 10⁻³ pfu/cell with PR8 influenza virus and infective particles analyzed by plaque assay. Three independent experiments were performed. ns P > 0.05; *P < 0.05; **P < 0.01; ***P < 0.001.