Figure 7.
Bcor insufficiency causes reduction in H2AK119ub1 levels. (A) Scatter plots showing the correlation of the fold enrichment values of H2AK119ub1 against the input signals (ChIP/input) (TSS ± 2.0 kb of RefSeq genes) in GMPs from ΔE9-10, ΔTet2, and DKO mice 4 weeks after the tamoxifen treatment relative to WT GMPs. The light diagonal lines represent the boundaries for 1.5-fold increase or decrease in fold enrichment of H2AK119ub1. We defined “PRC1 targets” as genes with H2AK119ub1 enrichment greater than twofold over the input signals. Among PRC1 targets, the genes that gained or lost H2AK119ub1 modifications >1.5-fold compared with those in WT are indicated in pink. (B) Venn diagrams showing the overlap of PRC1 target genes that lost H2AK119ub1 modifications >1.5-fold in ΔE9-10, ΔTet2, and DKO GMPs compared with those in WT GMPs in (A). (C) Heat map showing the levels of H2AK119ub1 at the range of TSS ± 5.0 kb. The levels of H2AK119ub1 in each cluster are plotted in upper columns. (D) Box-and-whisker plots showing H2AK119ub1 levels of genes in cluster 1 in WT, ΔE9-10, ΔTet2, and DKO GMPs. Boxes represent 25 to 75 percentile ranges. The whiskers extend to the most extreme data point which is no more than 1.5 times the interquartile range from the box. Horizontal bars represent medians. Mean values are indicated by “+” in red. ***P < .001 by the Student t test. (E) Snapshots of RNA sequencing and H2AK119ub1 ChIP-seq signals at the Hoxa7 and Hoxa9 gene loci in WT, ΔE9-10, ΔTet2, and DKO GMPs. The structure of the Hoxa7 and Hoxa9 genes are indicated at the bottom. (F) Manual ChIP quantitative PCR assays for H2AK119ub1 in GMPs and LSK cells at the Hoxa9 and Cebpa loci, respectively. The relative amounts of immunoprecipitated DNA are depicted as a percentage of input DNA. Data are shown as the mean ± SEM (n = 4). *P < .05; **P < .01 by the Student t test.

Bcor insufficiency causes reduction in H2AK119ub1 levels. (A) Scatter plots showing the correlation of the fold enrichment values of H2AK119ub1 against the input signals (ChIP/input) (TSS ± 2.0 kb of RefSeq genes) in GMPs from ΔE9-10, ΔTet2, and DKO mice 4 weeks after the tamoxifen treatment relative to WT GMPs. The light diagonal lines represent the boundaries for 1.5-fold increase or decrease in fold enrichment of H2AK119ub1. We defined “PRC1 targets” as genes with H2AK119ub1 enrichment greater than twofold over the input signals. Among PRC1 targets, the genes that gained or lost H2AK119ub1 modifications >1.5-fold compared with those in WT are indicated in pink. (B) Venn diagrams showing the overlap of PRC1 target genes that lost H2AK119ub1 modifications >1.5-fold in ΔE9-10, ΔTet2, and DKO GMPs compared with those in WT GMPs in (A). (C) Heat map showing the levels of H2AK119ub1 at the range of TSS ± 5.0 kb. The levels of H2AK119ub1 in each cluster are plotted in upper columns. (D) Box-and-whisker plots showing H2AK119ub1 levels of genes in cluster 1 in WT, ΔE9-10, ΔTet2, and DKO GMPs. Boxes represent 25 to 75 percentile ranges. The whiskers extend to the most extreme data point which is no more than 1.5 times the interquartile range from the box. Horizontal bars represent medians. Mean values are indicated by “+” in red. ***P < .001 by the Student t test. (E) Snapshots of RNA sequencing and H2AK119ub1 ChIP-seq signals at the Hoxa7 and Hoxa9 gene loci in WT, ΔE9-10, ΔTet2, and DKO GMPs. The structure of the Hoxa7 and Hoxa9 genes are indicated at the bottom. (F) Manual ChIP quantitative PCR assays for H2AK119ub1 in GMPs and LSK cells at the Hoxa9 and Cebpa loci, respectively. The relative amounts of immunoprecipitated DNA are depicted as a percentage of input DNA. Data are shown as the mean ± SEM (n = 4). *P < .05; **P < .01 by the Student t test.

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