Figure 6

Candidate regulators of TAL1-bound active enhancers. (A) Motifs that distinguish TAL1 OSs that are active enhancers from those that are inactive. The motif discovered by DME2 is given on the first line of each box, followed by the known TF binding site motifs discovered by TOMTOM, all shown as aligned logos. (B) Motifs that distinguish TAL1 OSs that are inactive enhancers from those that are active. (C) Venn diagrams show genome-wide overlaps between SMAD1, TAL1, and GATA1 peaks in erythroid lineage, G1E-ER4 + E2 cells. Number of regions bound by these peaks is shown. (D) Power of SMAD1 binding on enhancer activity in transgenic mice. (E) Heat map depicting the effect of co-localization of SMAD1, TAL1, and GATA1 in different combinations on success rate in vitro enhancer assay (transfections into hematopoietic cell line). (F) Shown is an intron of the Gypc gene in the mouse genome, along with ChIP-seq binding profiles for TAL1 (GEO sample numbers: GSM746555-56, GSM746571-72, GSM746583_84), GATA1 (GSM453997, GSM417015, GSM1151146, GSM746581-82), GATA2 (GSM641911, GSM722387), GATA4 (GSM558904), SMAD1 (GSM722388, GSM722391), STAT1 (GSM994528), STAT5 (GSM652878), STAT5b (GSM1014575, GSM671418), IRF4 (GSM1004833_35, GSM1004821), and FOXO1 (GSM1131775, GSM998924) in hematopoietic cells, in descending order. ChIP-seq binding signals (bigwig) were obtained from CODEX [59].