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HMGN1 and HMGN2 are recruited to acetylated and histone variant H2A.Z-containing nucleosomes to regulate chromatin state and transcription

ABSTRACT: The High Mobility Group Nucleosome-binding (HMGN) proteins are small abundant nuclear proteins that directly bind nucleosomes and constitute a major component of chromatin. HMGN proteins specifically localize to enhancers and actively transcribed genes across the genome, however the roles of HMGN proteins in regulating chromatin structure and transcription remain poorly understood. To investigate the localization and function of HMGN proteins on chromatin, we engineered mouse embryonic stem cells (mESCs) lacking HMGN1 and/or HMGN2 (Hmgn1-/- mESCs, Hmgn2-/- mESCs, and Hmgn1-/-Hmgn2-/- mESCs) and profiled gene expression and localization of architectural proteins. ChIP-sequencing was performed for the RAD21 subunit of cohesin and CTCF to assess the functional implications of loss of HMGN1 and HMGN2 on cohesin and CTCF localization.

ORGANISM(S): Mus musculus

PROVIDER: GSE291947 | GEO | 2025/11/21

REPOSITORIES: GEO

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HMGN1 and HMGN2 are recruited to acetylated and histone variant H2A.Z-containing nucleosomes to regulate chromatin state and transcription

Project description:The High Mobility Group Nucleosome-binding (HMGN) proteins are small abundant nuclear proteins that directly bind nucleosomes and constitute a major component of chromatin. HMGN proteins specifically localize to enhancers and actively transcribed genes across the genome, however the roles of HMGN proteins in regulating chromatin structure and transcription remain poorly understood. To investigate the localization and function of HMGN proteins on chromatin, we engineered mouse embryonic stem cells (mESCs) lacking HMGN1 and/or HMGN2 (Hmgn1-/- mESCs, Hmgn2-/- mESCs, and Hmgn1-/-Hmgn2-/- mESCs) and profiled gene expression and localization of architectural proteins. Gene expression was profiled in WT mESCs, Hmgn1-/- mESCs, Hmgn2-/- mESCs, and Hmgn1-/-Hmgn2-/- mESCs via RNA-sequencing.

2025-11-21 | GSE291949 | GEO

HMGN1 and HMGN2 are recruited to acetylated and histone variant H2A.Z-containing nucleosomes to regulate chromatin state and transcription

Project description:The High Mobility Group Nucleosome-binding (HMGN) proteins are small abundant nuclear proteins that directly bind nucleosomes and constitute a major component of chromatin. HMGN proteins specifically localize to enhancers and actively transcribed genes across the genome, however the roles of HMGN proteins in regulating chromatin structure and transcription remain poorly understood. To investigate the function of HMGN proteins on chromatin, we engineered mouse embryonic stem cells (mESCs) lacking HMGN1 and/or HMGN2 (Hmgn1-/- mESCs, Hmgn2-/- mESCs, and Hmgn1-/-Hmgn2-/- mESCs) and performed mass spectrometry-based quantification of a panel of histone residue states to quantify the levels of specific histone modifications in WT and Hmgn1-/-Hmgn2-/- mESCs.

2025-11-22 | PXD070369 | Pride

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.

2017-10-01 | GSE66442 | GEO

Epigenetic Regulation of Ameloblast Differentiation by HMGN Proteins

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.

2024-02-14 | GSE226942 | GEO

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.

2022-10-19 | GSE193462 | GEO

Recruitment of HMGN By H3K27ac Modified Nucleosomes to Regulatory Sites Modulates Transcription Factor Binding to Chromatin

Project description:H3K27ac modified nucleosomes are a major epigenetic mark of active chromatin that can be used to identify cell type specific chromatin regulatory regions which serve as binding sites for transcription factors. Here we show that H3K27ac modified nucleosomes recruit the ubiquitous nucleosome binding proteins HMGN1 and HMGN2 to cell-type specific chromatin regulatory regions. We find that HMGNs bind directly to the acetylated nucleosome and that the H3K27ac residue and linker DNA are necessary and sufficient for the preferential binding of HMGNs to the modified nucleosomes. Loss of HMGNs increases the levels of H3K27me3 and the histone H1 occupancy at enhancers and promoters and alters the interaction of several transcription factors with chromatin. These experiments identify an additional mechanism whereby the H3K27ac epigenetic mark promotes chromatin decompaction and provide insights into the molecular mechanism whereby HMGN proteins, which bind to chromatin without DNA sequence specificity, modulate cell type specific gene expression.

2020-09-20 | GSE156697 | GEO

Systematic assessment of ISWI subunits reveals that NURF creates local accessibility for proper CTCF function

Project description:Catalytic activity of the ISWI family of remodelers is critical for nucleosomal organization and transcription factor binding, including the insulator protein CTCF. To define which subcomplex mediates these diverse functions we phenotyped a panel of isogenic mouse stem cell lines each lacking one of six ISWI accessory subunits. Individual deletions of either CERF, RSF1, ACF, WICH or NoRC subcomplexes only moderately affect the chromatin landscape, while removal of the NURF-specific subunit BPTF leads to drastic reduction in chromatin accessibility and Snf2h ATPase localization around CTCF sites. While this reduces distances to the adjacent nucleosomes it only modestly impacts CTCF binding itself. In absence of accessibility, the insulator function of CTCF is nevertheless impaired resulting in lower occupancy of cohesin and cohesin-loading factors, and reduced insulation at these sites, highlighting the need of NURF-mediated remodeling for open chromatin and proper CTCF function. Our comprehensive analysis reveals a specific role for NURF in mediating Snf2h localization and chromatin opening at bound CTCF sites showing that local accessibility is critical for cohesin binding and insulator function.

2024-03-13 | PXD042945 | Pride

Cohesin recruitment to promoters and enhancers by general transcription factors and chromatin regulators

Project description:Background Cohesin is a major regulator of three-dimensional genome organization and gene expression. Cohesin binds to DNA and dynamically extrudes a DNA loop, often bringing two cis-regulatory elements physically close together. Extruding cohesin molecules can be stalled or stabilized when they encounter a CTCF insulator protein on DNA, thereby anchoring a DNA loop. However, many enhancer-promoter loops that are bound by cohesin lack CTCF and it is not clear how cohesin is recruited to these sites in the genome. Results Here, we investigate the localization patterns of cohesin, as well as general chromatin state and localization of transcription factors WDR5, SP1, and NFYA in mouse embryonic stem cells. The SP1 and NFYA transcription factors are ubiquitously expressed proteins known to regulate expression of genes associated with a variety of cellular processes, while WDR5 is a core component of multiple complexes that regulate chromatin. Cohesin co-binds promoters and enhancers with WDR5, with SP1, or with NFYA in mESCs and other cell types. Cohesin co-immunoprecipitates with WDR5, SP1, and NFYA and cohesin simultaneously binds to the same chromatin molecules with these proteins. At co-bound sites, depletion of cohesin does not alter binding of WDR5, SP1, or NFYA;, however depletion of WDR5, SP1, or NFYA decreases cohesin binding. Conclusions These results indicate that general transcription factors and chromatin regulators recruit cohesin to specific sites in chromatin and thereby serve as structural regulators of enhancer-promoter loops via the recruitment of cohesin.

2025-06-09 | GSE283958 | GEO

Expression data from human HMGN4- and HMGN2-expressing mouse embryionic fibroblasts

Project description:HMGN proteins, a family of non-histone nucleosome-binding proteins, maintain a dynamic balance between more and less compacted fibers via interactions with other architectural elements of chromatin. This balance affects the ability of regulatory factors to access their target sites, which eventually modifies the expression profile of the cell. We used microarrays to detail gene expression change in mouse fibroblasts overexpressing human HMGN4 to identify outlier genes and distinct classes of up- and down-regulated genes during this process. Mouse embryonic fibroblasts (MEFs), MEFs, expressing hHMGN4 (MEF-N4) or hHMGN2 (MEF-N2) or vector alone (MEF-V, served as a control) were harvested from exponentially grown cell culture for RNA extraction and hybridization on Affymetrix microarrays.

2016-08-01 | E-GEOD-83313 | biostudies-arrayexpress

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