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. Author manuscript; available in PMC: 2016 May 7.
Published in final edited form as: Cell. 2015 May 7;161(4):774–789. doi: 10.1016/j.cell.2015.04.034

Figure 4. Genomic instability in RNA exosome deficient ES cells along with accumulation of DNA/RNA hybrids and loss of chromatin silencing markers H3K9me2 and HP1γ at x-eRNA expressing sequences.

Figure 4

(A) γH2AX immunoprecipitation for DNA double strand breaks at enhancer sequences resident in the Bcl6 (left), Cd38 (middle), and Klf6 (right) loci in wild-type, Exosc10COIN/LacZ, and Exosc3COIN/COIN ES cells following ionizing radiation treatment. (B) DNA/RNA hybrid immunoprecipitation at Ncoa3 (left), Cd38 (middle), and Klf6 (right) enhancers in wild-type, Exosc10COIN/LacZ, and Exosc3COIN/COIN ES cells. (C) Immunoprecipitation for heterochromatin marker H3K9me2 at enhancer sequences resident in the Bcl6 (left), Cd38 (middle), and Klf6 (right) loci in wild-type, Exosc10COIN/LacZ, and Exosc3COIN/COIN ES cells. (D) Immunoprecipitation for heterochromatin marker HP1γ at enhancer sequences resident in the Bcl6 (left), Cd38 (middle), and Klf6 (right) loci in wild-type, Exosc10COIN/LacZ, and Exosc3COIN/COIN ES cells. Each plot is a representation of three independent experiments performed (*P<0.05; **P<0.01 by t-test). See Figure S4.