Figure 1
Figure 1. Genome-wide identification of Hoxa9 and Meis1 binding sites in leukemia cells. (A) Schematic diagram of Hoxa9 and Meis1 binding site identification. Two replicate sequencing runs were performed for each factor, and the enriched regions (or peaks) were selected only if they were detected in both biologic replicates, consistent with ENCODE Consortium standard. The peaks from both factors were subsequently merged into one set of peaks (n = 825). Notably, a total of 52% of Hoxa9 peaks overlap with Meis1 peaks and 33% of Meis1 peaks overlap with Hoxa9 peaks. (B) Characterization of genomic localization of Hoxa9 and Meis1 binding sites. (C) Cumulative distribution of genomic localization indicates that Hoxa9 (red) and Meis1 (blue) binding sites are significantly (Kolmogorov-Smirnov test) closer to transcription start sites, compared with control peaks (gray).

Genome-wide identification of Hoxa9 and Meis1 binding sites in leukemia cells. (A) Schematic diagram of Hoxa9 and Meis1 binding site identification. Two replicate sequencing runs were performed for each factor, and the enriched regions (or peaks) were selected only if they were detected in both biologic replicates, consistent with ENCODE Consortium standard. The peaks from both factors were subsequently merged into one set of peaks (n = 825). Notably, a total of 52% of Hoxa9 peaks overlap with Meis1 peaks and 33% of Meis1 peaks overlap with Hoxa9 peaks. (B) Characterization of genomic localization of Hoxa9 and Meis1 binding sites. (C) Cumulative distribution of genomic localization indicates that Hoxa9 (red) and Meis1 (blue) binding sites are significantly (Kolmogorov-Smirnov test) closer to transcription start sites, compared with control peaks (gray).

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