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. Author manuscript; available in PMC: 2023 Aug 18.
Published in final edited form as: Cell Chem Biol. 2022 Jul 14;29(8):1273–1287.e8. doi: 10.1016/j.chembiol.2022.06.007

Figure 6. BCL11A represses HBG1/2 genes independently of promoter CpG methylation.

Figure 6.

% CpG methylation at 8 CpG sites in HBG1/2 promoters at d4 (a), d6 (b), and d9 (c) of differentiation in DMSO (blue dots) and dTAG-47 (red dots) treated BCL11AFKBP cells, as compared to d0. Extent of HBG upregulation shown in orange, red, maroon arrows., n=2 d. HBG1/2 promoter CpG methylation in differentiating BCL11AFKBP cells treated with azacytidine (0μM, 0.1μM, and 0.3μM) and DMSO or dTAG-47. Dots are CpGs, and color intensity indicates % methylation. e. Total promoter CpG methylation represented as the euclidean distance of CpG-methylation values from the methylation pattern at d0, for DMSO or dTAG-47 treatments in conjunction with azacytidine (0μM, 0.1μM and 0.3μM). f. RT-qPCR quantification of HBG1/2 as a percent of total globin RNA in differentiating BCL11AFKBP cells treated with azacytidine (0μM, 0.1μM and 0.3μM) in combination with DMSO (black bars) or dTAG-47 (open bars). HPRT is endogenous control, %HBG = 100* [HBG/ (HBG+HBB)]. See also Figure S5.