Fig. 1
From: Robust hematopoietic specification requires the ubiquitous Sp1 and Sp3 transcription factors
The complete absence or the truncation of Sp1 do not cause widespread changes in chromatin accessibility. a Schematic representing in vitro differentiation of ESC. b FACS analysis of Flk1 expression in E14 WT and E14 Sp1ΔDBD/ΔDBD cells derived from embryoid bodies (EB) at day 3.25 of in vitro differentiation. Left panel: representative FACS profiles for Flk1-PE staining, right panel: graph showing Flk1 expression and isotype controls for E14 WT and Sp1ΔDBD/ΔDBD cells (n = 4, **indicates p < 0.001). c Graph showing the percentage of EB releasing macrophages in a macrophage release assay (n = 3, * indicates p < 0.05). d Rescue of Flk1 expression levels by re-expression of wild-type Sp1 in Sp1−/− and Sp1ΔDBD/ΔDBD cells (n = 3 for Sp1−/− and n = 4 for Sp1ΔDBD/ΔDBD, p values are indicated on the graph). e Pearson correlation plot of accessible chromatin regions in ESC as determined by ATAC-seq, in WT cells and Sp1 mutant ESC clones. f Heat maps showing the fold difference in accessible chromatin sites, as determined by ATAC, between WT and Sp1ΔDBD/ΔDBD E14 ESC (left panel) and WT and Sp1−/− A17Lox ESC (right panel). The red box indicates WT-specific ATAC sites, while the blue box indicates ATAC sites specific to either Sp1ΔDBD/ΔDBD or Sp1−/− cell lines