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. 2016 Mar 30;9:13. doi: 10.1186/s13072-016-0062-8

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© Panday and Grove. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 8 — Dynamic chromatin environment in hmo1∆ that leads to faster chromatin remodeling and DSB repair is restored to wild-type levels by expression of H1. a Survival of DDY3, hmo1∆, hmo1-AB and the corresponding strains expressing H1. After DSB induction, cells were plated and colonies counted. Three independent experiments were performed. Error bars represent standard deviation. b Cells not induced to express HO were plated as control. c qRT-PCR analysis of ChIP using antibody to phosphorylated H2A, monitoring presence of γ-H2AX at MAT during DNA damage (galactose) and repair (glucose). Data are normalized to corresponding input control at each time point. d qRT-PCR analysis of ChIP using antibody to Arp5, monitoring presence at MAT (left panel) and 3.1 kb downstream of DSB (right panel) during DNA damage (galactose) and repair (glucose). Data are normalized to corresponding input control at each time point. Three independent experiments were performed. Error bars represent standard deviation. In all panels, asterisks represent statistical significance from DDY3 at the respective time points based on Student’s t test (P < 0.05)