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. 2018 Jan 19;8:1230. doi: 10.1038/s41598-018-19370-6

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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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Influenza virus replication increases in Dot1L downregulated cells. A549 cells were treated with Dot1L inhibitor (48 h) or transduced with lentiviruses expressing shRNA specific for Dot1L (shDot1L 1, shDot1L 2) or an irrelevant shRNA (shTM) (5 days). The H3K79 methylation levels were analyzed by Western blot (A), or colorimetric analysis (B). A549 cells, uninfected or transduced with control or specific Dot1L silencers during 5 days, were infected with PR8hv (C) or CAL07 (D) strains at m.o.i. 10⁻³. Virus titer was determined by plaque assay on MDCK cells at indicated hpi. Student’s t test with Welch’s correction; 3 technical replicates of 3 independent experiments were performed.