Figure 4.
CBS7/9+/−alters enhancer/promoter accessibility and interactome in the HOXA locus. (A-C) ATAC-seq analysis of the alteration in chromatin accessibility upon the heterozygous deletion of the CBS7/9 boundary site in MOLM13 cells. Shown are altered chromatin accessibility in the HOXA (A), RUNX1 (B), and ZEB1 (C) loci compared with the WT control and the CBS7/9+/− clone. (D) Long-range chromatin interactions from HOXA9 gene, as determined by 4C-seq analysis, compared with WT and CBS7/9+/− MOLM13 cells. The red arrow indicates that HOTTIP interacts with HOXA9 in WT cells, and the interaction is reduced in CBS7/9+/− cells. (E) Changed interaction between the HOXA9 and ZEB1 genes, as determined by 4C-seq analysis, compared with WT and CBS7/9+/− MOLM13 cells.

CBS7/9+/−alters enhancer/promoter accessibility and interactome in the HOXA locus. (A-C) ATAC-seq analysis of the alteration in chromatin accessibility upon the heterozygous deletion of the CBS7/9 boundary site in MOLM13 cells. Shown are altered chromatin accessibility in the HOXA (A), RUNX1 (B), and ZEB1 (C) loci compared with the WT control and the CBS7/9+/− clone. (D) Long-range chromatin interactions from HOXA9 gene, as determined by 4C-seq analysis, compared with WT and CBS7/9+/− MOLM13 cells. The red arrow indicates that HOTTIP interacts with HOXA9 in WT cells, and the interaction is reduced in CBS7/9+/− cells. (E) Changed interaction between the HOXA9 and ZEB1 genes, as determined by 4C-seq analysis, compared with WT and CBS7/9+/− MOLM13 cells.

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