Project description:To gain insight into how miR-142 deficit drives a BC-like transformation, we performed RNA-seq on bone marrow (BM) Lin-Sca-1+c-Kit+ cells (LSKs) harvested from normal miR-142+/+ (wt) and miR-142−/− (miR-142 KO) mice, as well as from leukemic miR-142+/+ BCR-ABL (CP CML) and miR-142−/− BCR-ABL (BC CML) mice, two weeks after BCR-ABL induction. We then performed gene expression profiling analysis using data obtained from RNA-seq of 24 samples of LSK cells from 4 mouse strains (KO vs WT, KO CML vs CML).
Project description:2 types of dendritic cells (DCs) can be generated in vitro in the presence of Flt3-L: CD4+ equivalent CD24- DCs and CD8+ equivalent CD24+ DCs. miR-142-/- mice show a severe defect in the generation of CD4+ equivalent CD24- DCs. To understand the underlying mechanism, RNA expression was analyzed by Affymetrix microarray from the 2 in vitro subtypes of DCs derived from miR-142+/+ and miR-142-/- bone marrow cells. We used microarrays to detail the global programme of gene expression in the presence or absence of miR-142 in in vitro derived DCs. Bone marrow cells from miR-142+/+ and miR-142-/- C57Bl/6 mice were isolated and incubated in the presence of Flt3-L for 8 days. in vitro derived wt and ko dendritic cells were devided into CD4+ and CD8+ equivalent DCs by FACS and sorted with a FACS-Aria. RNA was isolated and gene expression was investigated
Project description:ATAC-seq profiling of Nfat5 KO and wild type macrophages derived from bone marrow (primary cells), treated or not with Lipopolysaccharide (LPS).
