Fig. 3: Chromatin accessibility analysis unveils E2F1 as a transcriptional activator of H2AZ2. | Cell Death & Differentiation

Fig. 3: Chromatin accessibility analysis unveils E2F1 as a transcriptional activator of H2AZ2.

From: E2F and STAT3 provide transcriptional synergy for histone variant H2AZ activation to sustain glioblastoma chromatin accessibility and tumorigenicity

Fig. 3

A Heatmaps displaying the differences in ATAC-Seq signal after H2AZ2 KD. The panels on top of the heatmaps show the average signal for each group of regions in each individual sample. B Barplot showing the log2 enrichment of the observed over expected overlap of genomic regions with differential ATAC-Seq signal upon H2AZ2 KD as shown in (A). C Western blot analysis of H3K27ac, H3K4me3, H3K9me3 proteins levels upon H2AZ2 KD of GSC. Histone H3 serves as the loading control. D Venn diagram showing the 992 high confidence H2AZ2-associated gene targets from the intersection between the H2AZ ChIP-Seq and ATAC-Seq analysis upon H2AZ2 KD. E Transcription factor enrichment analysis (ReMap software) within the significantly decreased ATAC-seq peaks upon H2AZ2 KD. F Correlative analysis of H2AZ2 levels with that of E2F1 or E2F4 in glioma patients from TCGA and REMBRANDT cohorts. G ChIP-qPCR analysis of E2F1 occupancy and H3K27ac levels on the H2AZ2 promoter in H2AZ2 depleted GSC (n = 3) (mean ± SD). ***p < 0.005. H qRT-PCR analysis of H2AZ2 and H2AZ1 mRNA levels in E2F1 KD GSC. HSP70 and TBP serve as the housekeeping genes (n = 3) (mean ± SD). *p < 0.05; **p < 0.005. I Western blot analysis of E2F1 and H2AZ protein levels upon E2F1 KD in GSC. J Quantification of H2AZ band intensities in (I) when normalized to the β-actin control (n = 3) (mean ± SD). **p < 0.005. G, H, J Two-tailed unpaired Student’s t test.

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