Fig 2: TRIM33 ChIP-seq analysis in 38B9, AML, and T-ALL.(A) Ranking of TRIM33 occupied sites based on average tag counts obtained from ChIP-seq analysis in the indicated cell lines. The regions shown represent the reproducible peaks identified in each of two independent biological replicates. The Bim-117 and Atp1b3-35 regions are as indicated in 38B9 and AML. In T-ALL we did not identify these regions as robust peaks and instead we labeled the top two outlier TRIM33 peaks in this cell type. (B) MEME-based motif analysis at 400 bp windows centered on TRIM33 occupied peaks shown in A. The distribution of motifs in this window is indicated on the right.DOI: http://dx.doi.org/10.7554/eLife.06377.010

Fig 3: (A–B) TRIM33 ChIP-seq occupancy profiles at the Bim locus (A) and the Atp1b3 locus (B) in the indicated cell types.Validated transcript models from the mm9 genome assembly are depicted below.DOI: http://dx.doi.org/10.7554/eLife.06377.007

Fig 4: ChIP-qPCR of TRIM33 and PU.1 in 3 independent MLL-AF9/NrasG12D acute myeloid leukemia cell lines, which are all early passage cultures derived from leukemic mice.DOI: http://dx.doi.org/10.7554/eLife.06377.023

Fig 5: Additional experiments evaluating the role of TRIM33 in AML and T-ALL.(A) RT-qPCR analysis of Bim mRNA levels following TRIM33 shRNA transduction into the indicated cell lines. Plotted is the average of three biological replicates. Results were normalized to Gapdh. (B) ChIP-seq occupancy profile of H3K27 acetylation in the indicated cell lines. Arrows indicate the location of the Bim-117 and -66 regions (see text). The H3K27ac ChIP-seq data from AML was derived from (Shi et al., 2013).DOI: http://dx.doi.org/10.7554/eLife.06377.018