Fig. 7: PML1 regulates H3K4me3 marks and is critical in recruiting WDR5, MLL1, and MLL2. | Cell Death & Differentiation

Fig. 7: PML1 regulates H3K4me3 marks and is critical in recruiting WDR5, MLL1, and MLL2.

From: The PML1-WDR5 axis regulates H3K4me3 marks and promotes stemness of estrogen receptor-positive breast cancer

Fig. 7

A Heatmap illustrating changes in H3K4me3 binding sites across PML-bound promoters following PML loss. Heatmaps show representative data from triplicate experiments, while meta-plots illustrate outcomes from triplicate experiments. B ChIP-seq tracks reveal H3K4me3 distribution on JAG1, KLF4, MYC, SNAI1, and YAP1 genes, with and without PML-knockdown, while genomic tracks depict aggregated outcomes from triplicate experiments. C Loss of PML significantly reduces the H3K4me3 mark. D PML1, not PML4, restores H3K4me3 marks on BCSC-related gene promoters in PML knockdown cells. PML1 is required for the associations of WDR5 (E), MLL1 (F), and MLL2 (G) with the stemness gene promoters. Loss of WDR5 reduces the expression of the stemness genes (H) and the H3K4me3 (I) mark on their promoters but has little or no effect on PML associations with these gene promoters (J). The data were analyzed using Two-way ANOVA. Each experiment was performed with N = 3 in each group.

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