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Epigenetic changes in ΔTXR1 cells: response to replication stress. Multiple histone PTMs in crosstalk with H3K27 methylation, including hyper-acetylation (H2A, H2A.Z, and H4), hyper-methylation (particularly at H3K56), and γH2A.X (H2A.X S134 phosphorylation). They are potentially underlain by DNA damage response to replication stress in ΔTXR1 cells, modulated by ATR, NuA4, and H2A.Y. ac: acetylation; me1: mono-methylation; ph: phosphorylation. See text for details.
