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Epigenetic Regulation of Ameloblast Differentiation by HMGN Proteins

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE226942 | GEO | 2024/02/14

REPOSITORIES: GEO

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HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity [RNA-Seq]

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.

2022-10-19 | GSE193338 | GEO

HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity [scRNA-Seq]

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.

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HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity [ATAC-Seq]

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HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity [ChIP-Seq]

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Genome-wide expression profiling analysis of a Hmgn2 and Hmgn1/2 double knock out mutant mouse model

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.

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Epigenetic Regulation of Ameloblast Differentiation by HMGN Proteins

Project description:Epigenetic Regulation of Ameloblast Differentiation by HMGN Proteins

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Transcriptome of human odontoblast, pre-secretory ameloblast and secretory ameloblast

Project description:The goal of the study was to characterize the whole genome transcriptome profiles of human ameloblasts and odontoblasts, evaluate molecular pathways and advance our knowledge of the human tooth development. We found that during primary tooth formation, odontoblasts expressed 14,802 genes, presecretory ameloblasts 15,179 genes and secretory ameloblasts 14,526 genes. Four human fetuses were obtained at ages 15-20 weeks gestation, immediately placed on ice and the tooth buds dissected from the jaws, placed in RNAlater and refrigerated at 4C for 1-4 weeks to allow decalcification by EDTA. The tissue was then frozen and stored at -80C. The tissue was sectioned at -35C at a thickness of 7 microns. These sections were used for laser capture microdissection (LCM) to isolate the human odontoblasts and ameloblasts in different stages of enamel formation, using static image settings. In total, 4 odontoblast, 4 pre-secretory ameloblast and 4 secretory ameloblast pooled samples were used for RNA extraction and microarray analysis.

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The Pitx2:miR-200c/141:noggin pathway regulates BMP signaling and ameloblast differentiation

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2013-07-09 | E-GEOD-48583 | biostudies-arrayexpress

Single-cell RNA-seq analysis of rat molars reveals cell-identity and driver genes associated with dental mesenchymal cell differentiation

Project description:To explore the cell-identity and driver genes related to dental mesenchymal cell differentiation during the late bell hard tissue formation stage, the first and second mandibular molars (M1 and M2) of rat at postnatal days 5 were dissected for enzymatic digestion and subjected to single-cell RNA sequencing (scRNA-seq).

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Single-cell RNA-sequencing from mouse incisor reveals dental epithelial cell-type specific genes

Project description:Dental epithelial stem cells give rise to all dental epithelial cell types, inner enamel epithelium, outer enamel epithelium, ameloblasts, stratum intermedium and stellate reticulum to form enamel. These all types of epithelial cells have distinct roles and are essential for enamel formation. These cell types are conventionally classified by their cell shape, however, the transcriptome and biological roles of each cell types are not fully understood. Here, we used single-cell RNA-sequencing to clarify the heterogeneity of dental epithelial cell types. Unbiased clustering of 6260 single-cells from post-natal day 7 mouse incisors are classified into 4 dental epithelial and 2 mesenchymal populations; 2 clusters of ameloblast, IEE/OEE and SI/SR clusters. Secretory-stage of ameloblasts were divided into Dspp+ or Ambn+ ameloblast. Pseudo-time analysis indicated that Dspp+ ameloblast differentiate into Ambn+ ameloblast. Further, Dspp and Ambn would be stage-specific markers of ameloblast. Gene Ontology (GO) analyses of each clusters indicate potent roles of cell types; OEE in regulation of tooth size and SR in transport of nutrition. Moreover, we identified novel dental epithelial cell marker genes, Pttg1, Atf3, Cldn10 and Krt15. These results provide a resource of transcriptome data in dental cells and contribute further molecular analyses of enamel formation.

2020-09-23 | GSE146855 | GEO

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