Figure 1. Diminished H3K9me2 at IFN and IFN-inducible genes (ISGs) in DCs compared with MEFs. (A) H3K9me2 levels and distribution at the Ifnb1 and Mx1 gene loci in WT MEFs and in splenic DCs from WT and IFNAR1−/− mice. The gene fragments associated with H3K9me2 were identified and quantified by ChIP-Seq analysis. Y-axes represent the number of reads per million mapped reads per 25 bp window. (B) Scatter plots display relative FPKM (fragments per kb per million mapped reads) values of H3K9me2 or H3K4me3 for individual ISGs in WT MEFs (x-axes) and splenic DCs (y-axes). ChIP-Seq represents three independent experiments for MEFs and two experiments for DCs. (C) Abundance of H3K9me2 at ISGs and poly I:C–inducible genes and non-ISG proinflammatory genes in MEFs and DCs. FPKM values of H3K9me2 for ISGs in WT MEFs (left) and splenic DCs (right). ChIP-Seq represents three independent experiments for MEFs and two experiments for DCs. The horizontal bars represent the mean ± SEM. (D) H3K9me2 levels and distribution at the indicated genes in MEFs and DCs. The gene fragments associated with H3K9me2 were identified and quantified by ChIP-Seq analysis. Y-axes represent the number of reads per million mapped reads. (E) Abundance of H3K9me2 at the Ifnβ promoter in mouse and human cells of various types (left and right, respectively). The levels of H3K9me2 at the Ifnβ promoters in different cells types were evaluated by ChIP-qPCR analysis. H3K9me2 was normalized to total histone H3 levels. Data are representative of two independent experiments. Card. Myoc., cardiac myocyte; Neurobl., neuroblastoma; BMDM, BM-derived macrophage; BMDC, BM-derived DC; pDC, splenic pDC; cDC, splenic conventional DC; HLF, human lung fibroblast; MoDC, monocyte-derived DC. Error bars are SD. Data are representative of two independent experiments. (F) Expression of G9a, GLP, H3K9me2, and total H3 in WT MEFs and splenic DCs. The expression of the indicated proteins was determined by Western blotting of nuclear extracts. Lamin B serves as a loading control. M.W., molecular weight. Data are representative of at least three independent experiments.
Figure 1.

Diminished H3K9me2 at IFN and IFN-inducible genes (ISGs) in DCs compared with MEFs. (A) H3K9me2 levels and distribution at the Ifnb1 and Mx1 gene loci in WT MEFs and in splenic DCs from WT and IFNAR1−/− mice. The gene fragments associated with H3K9me2 were identified and quantified by ChIP-Seq analysis. Y-axes represent the number of reads per million mapped reads per 25 bp window. (B) Scatter plots display relative FPKM (fragments per kb per million mapped reads) values of H3K9me2 or H3K4me3 for individual ISGs in WT MEFs (x-axes) and splenic DCs (y-axes). ChIP-Seq represents three independent experiments for MEFs and two experiments for DCs. (C) Abundance of H3K9me2 at ISGs and poly I:C–inducible genes and non-ISG proinflammatory genes in MEFs and DCs. FPKM values of H3K9me2 for ISGs in WT MEFs (left) and splenic DCs (right). ChIP-Seq represents three independent experiments for MEFs and two experiments for DCs. The horizontal bars represent the mean ± SEM. (D) H3K9me2 levels and distribution at the indicated genes in MEFs and DCs. The gene fragments associated with H3K9me2 were identified and quantified by ChIP-Seq analysis. Y-axes represent the number of reads per million mapped reads. (E) Abundance of H3K9me2 at the Ifnβ promoter in mouse and human cells of various types (left and right, respectively). The levels of H3K9me2 at the Ifnβ promoters in different cells types were evaluated by ChIP-qPCR analysis. H3K9me2 was normalized to total histone H3 levels. Data are representative of two independent experiments. Card. Myoc., cardiac myocyte; Neurobl., neuroblastoma; BMDM, BM-derived macrophage; BMDC, BM-derived DC; pDC, splenic pDC; cDC, splenic conventional DC; HLF, human lung fibroblast; MoDC, monocyte-derived DC. Error bars are SD. Data are representative of two independent experiments. (F) Expression of G9a, GLP, H3K9me2, and total H3 in WT MEFs and splenic DCs. The expression of the indicated proteins was determined by Western blotting of nuclear extracts. Lamin B serves as a loading control. M.W., molecular weight. Data are representative of at least three independent experiments.

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