GSE110566
Regulation of genes by HDAC2 via enzyme activity-independent manner during HL-60 cell differentiation by TPA
Human myeloid leukemia cell line, HL-60 cells, have a potential to differentiate into monocytes with treatment of 12-O-tetradecanoylphorbol-13-acetate (TPA). However, the underlying mechanism of differentiation by TPA is not fully elucidated yet. Here, we performed ChIP-seq profiling using RNA Pol II, HDAC2, AcH3 and H3K27me3, and analyzed the differential chromatin state changes during HL-60 differentiation by TPA. In this study, we focused on the atypical active genes, which showed enhanced H3 acetylation occupancies despite increased HDAC2 recruitment. We found that HDAC2 regulates the expression of these genes positively via histone deacetylase activity-independent manner. HDAC2 interacted and recruited Paired Box 5 (PAX5) to promoter of the target genes and regulated PAX5-mediated gene activation. Taken together, these data demonstrated the profiling of differentiation specific-chromatin status during the differentiation in HL-60 cells by TPA and suggested that HDAC2 activates certain genes through the interaction with PAX5 in enzyme activity independent pathway. Overall design: Genome binding/occupancy profiling of HDAC2, RNA PolII, acetyl-H3, H3K27me3 in differentiated-HL-60 cells