Project description:We report H3K27ac ChIP seq during time course of white preadipocyte browning from WT and HMGN1 and HMGN2 double knockout (DKO) mice .
Project description:We report mRNA seq during time course of white preadipocyte browning from WT and HMGN1 and HMGN2 double knockout (DKO) mice . Moreover, we support our finding that loss of HMGN promotes white adipocyte browning with RNA seq of WT and DKO MEFs transdifferentiation into brown-like adipocytes.
Project description:We report single-cell RNA seq (scRNA seq) at day 0 and day 6 of white preadipocyte browning from WT and HMGN1 and HMGN2 double knockout (DKO) mice. This supports our finding that loss of HMGN promotes white adipocyte browning with RNA seq of WT and DKO MEFs transdifferentiation into brown-like adipocytes.
Project description:To investigate the molecular mechanism of nucleosomal binding proteins HMGN regulating ameloblast differentiation We performed RNA-seq analysis of dental epithelium cells that were dissected from WT and DKO (Hmgn1-/-; Hmgn2-/-) mouse molars at three developmental stages.
Project description:DNase I hypersensitive sites (DHSs) are a hallmark of chromatin regions containing regulatory DNA such as enhancers and promoters; however, the factors affecting the establishment and maintenance of these sites are not fully understood. We now show that HMGN1 and HMGN2, nucleosome-binding proteins that are ubiquitously expressed in vertebrate cells, maintain the DHS landscape of mouse embryonic fibroblasts (MEFs) synergistically. Loss of one of these HMGN variants led to a compensatory increase of binding of remaining variant. Genome wide mapping of the DHSs in Hmgn1-/-, Hmgn2-/- and Hmgn1-/-n2-/- MEFs reveals that loss of both, but not a single HMGN variant, leads to significant remodeling of the DHS landscape, especially at enhancer regions marked by H3K4me1 and H3K27ac. Loss of HMGN variants affects the induced expression of stress responsive genes in MEFs, the transcription profiles of several mouse tissues, and leads to altered phenotypes that are not seen in mice lacking only one variant. We conclude that the compensatory binding of HMGN variants to chromatin maintains the DHS landscape and the transcription fidelity necessary to retain wild type phenotypes. Our studies provide insights into mechanisms that maintain regulatory sites in chromatin and into functional compensation among nucleosome binding architectural proteins.
Project description:Here we utilized a conditional knock-out mouse model to investigate the role of Smarca5, an ISWI subfamily chromatin remodeling ATPase, during thymocyte development using hCD2-iCre transgene. We did transcriptional profiling of FACS-sorted CD4/CD8 double-positive thymocytes as this thymic population was persistent yet strongly underrepresented in adult 6-week mutant thymi. Controls included age-matched CD4/CD8 double-positive thymocytes from wild-type and tumor suppressor protein Trp53-null mice. For comparison, the Smarca5/Trp53-double-deficient thymocytes included in the experiment were partially rescued upon loss of Trp53.
