Epigenetic profiling of mouse hematopoietic cells retrovirally transfected with MNX1 or empty vector (Ctr) from fetal liver or mouse bone marrow [ATAC-seq]

Acute myeloid leukemia (AML) results from aberrant hematopoietic processes and these changes are frequently initiated by chromosomal translocations. One particular subtype, AML with translocation t(7;12)(q36;p13), is found in children diagnosed before two years of age. The chromosomal breakage points of the t(7;12) have consistently been found to be located after exon 1 in the Motor neuron and pancreas homeobox 1 (MNX1) gene in chromosome 7, and after exon 2 in the ETV6 gene in chromosome 12. The aim of this study is the investigation of the leukomogenic potenial of MNX1 overexpression and MNX1-ETV6 fusion using mouse models, in addition to the molecular pathway through which MNX1 is inducing leukemia. Fetal liver hematopietic cells from C57BL/6 mice were retrovirally transfected with MNX1 and transplanted into 10-12 weeks old NOD.Cg-KitW-41J Tyr + Prkdcscid Il2rgtm1Wjl/ThomJ (NBSGW) mice. After establishment of leukmeia in the NBSGW mice, cells were collected from the bone marrow for ATAC and H3K27me3 Act-Seq. Negative control of fetal liver hematopietic cells from C57BL/6 mice retrovirally transfected with empty vector were used.