Changes in Ikaros binding and histone-modifications upon oncogenic ß-catenin activation [ChIP-Seq]

We find that, in contrast to most cancer types, beta-catenin activation in preB-ALL cells supresses proliferation and leads to cell death. Proteomic analyses indicate that unlike in solid tumors beta-catenin interacts with Ikaros factors (IKZF1 and IKZF3) in pre-B cells. In order to examine the interaction between IKZF1/IKZF3 and beta-catenin we performed ChIPseq to assay chromatin state and TF binding in CTNNB1-GOF and IKZF1/3-LOF conditions. Overall design: IKZF1, IKZF3, H3K27ac and H3K4me3 ChIP-seq was performed in pre-B cells from Ctnnb1Ex3fl/+ mice transformed with BCR-ABL1 and transfected with either non-targeting or IKZF1 and IKZF3 CRISPR/Cas9-RNP in order to study the effect of beta-catenin activation on IKZF1/3 binding and histone modifications in both IKZF1/3-WT and IKZF1/3-KO conditions.