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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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H3K79 methylation modulates replication of interferon-inducers viruses. A549 cells were plated alone or with Dot1L inhibitor (1 μM, 48 h) (A,C)), or transduced with lentiviruses expressing a control shRNA (TM), or specific Dot1L silencers (shTM, shDot1L 1, shDot1L 2, 5 days) (B,D). After that, the cells were infected with RSV (m.o.i. 1) (A,B) or VSV (m.o.i. 10^-3) (C,D). The inhibitor was present throughout the experiment in treated cells. Right panels show the corresponding expression of viral proteins and the indicated proteins measured by Western blot analysis. Virus titer was determined by plaque assay at indicated times post-infection. Student’s t test with Welch’s correction; 3 technical replicates of 3 independent experiments were performed.