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. 2020 Feb 10;11:809. doi: 10.1038/s41467-020-14595-4

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© The Author(s) 2020

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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Fig. 7 — a HU sensitivity was determined for WT and isogeneic set1Δ, bre2Δ, and spp1Δ strains, as well as the H3 strain and isogeneic H3K4A, H3R2A, H3K36A and H3K79A mutants. b Putative elevated H3K4me and c actual H3K4me3 after pTEF promoter was introduced into the CAN1 gene; error bars represent ± SEM (n = 3 technical replicates). Mutation rates of d native CAN1 (left panel) and pTEF-CAN1 (right panel) were measured by the fluctuation test (see Methods section) in RAD53-H3, RAD53-H3K4A, rad53-H3 and rad53-H3K4A cells. rad53 refers to rad53-K227A mutant. As in d, cells were treated by e 5 mM and f 100 mM HU. Data are the median with 95% confidence intervals (n = 11 independent samples). Statistical significance was determined by Mann–Whitney U-test; p < 0.05; asterisks represent p < 0.001 compared with RAD53-H3 or RAD53-H3K4A; ND, not determined.