IKAROS represses expression of BCL2L1 (BCL-XL) mRNA through recruitment of HDAC1. (A) HDAC1 binding sites at the BCL2L1 (BCL-XL) promoter were identified by ChIP-seq in Nalm6 cells. ChIP-seq data were analyzed with reference genome MRCh37 and the custom tracks are shown on CisGenome Browser. (B) IKAROS effects on the activity of the BCL2L1 promoter (−1 to −700 bp) were assessed by luciferase reporter assay in the presence of pan-HDACs inhibitor (TSA) or HDAC1 shRNA knockdown (shHDAC1). (C-E) The qChIP data showing binding of HDAC1 (C) and the presence of H3K9ac (D) and H3K27me3 (E) marks at the BCL2L1 promoter in Nalm6 and 697 B-ALL cells with IKAROS (IK) overexpression. (F-H) qChIP data showing binding of HDAC1 (F), H3K9ac (G), and H3K27me3 (H) at the BCL2L1 promoter in Nalm6 and 697 B-ALL cells with IKZF1 shRNA knockdown (shIK). ChIP enrichments are normalized to CTL-IgG samples. Cells were treated for 3 days; graphed data are the mean ± SD of triplicates representative of 1 of 4 independent experiments (C-H). *P < .05, **P < .01, ***P < .001, ****P < .0001. Ig, immunoglobulin.