Fig. 3: Loss of the MAZ binding site alters Hox gene expression pattern, chromatin domains and topological organization at Hox clusters. | Nature Genetics

Fig. 3: Loss of the MAZ binding site alters Hox gene expression pattern, chromatin domains and topological organization at Hox clusters.

From: CRISPR and biochemical screens identify MAZ as a cofactor in CTCF-mediated insulation at Hox clusters

Fig. 3

a, ChIP-seq for H3K27me3, H3K4me3, CTCF and MAZ in WT MNs and ChIP-seq for MAZ in MAZ KO MNs in the chromatin boundary of HoxA, HoxD and HoxC clusters. b, MAZ binding site deletion via CRISPR is depicted for the 5|6 site at the HoxA cluster. c, Heat map of relative gene expression in WT, CTCF(Δ5|6:6|7) and MAZ (Δ5|6) at the HoxA cluster in MNs versus ESCs from three biological replicates. d, RNA-seq MA plot of WT versus MAZ (∆5|6) ESCs (left) and MNs (right) from three biological replicates. HoxA genes are colored based on their position with respect to the previously demonstrated CTCF boundary in MNs. Hb9 is an MN marker. Differentially expressed genes are selected as P value adjusted < 0.05 using the Wald test built into DESeq2 (Supplementary Datasets 13 and 14). e, ChIP-seq for CTCF, MAZ, indicated histone modifications and RNA-seq tracks in WT and MAZ (∆5|6) ESCs and MNs in the HoxA cluster. ChIP-seq tracks are from one representative of two biological replicates for CTCF and MAZ and one replicate for the histone modifications. RNA-seq tracks are from one representative of three biological replicates. f, 4C contact profiles in WT versus MAZ (Δ5|6) ESCs and MNs using a viewpoint shown in red at indicated region at Hoxa5. One representative of three biological replicates is shown for all except for two replicates for WT MNs.

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