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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. Gene expression was profiled in WT mESCs, Hmgn1-/- mESCs, Hmgn2-/- mESCs, and Hmgn1-/-Hmgn2-/- mESCs via RNA-sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE291949 | 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. 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.

2025-11-21 | GSE291947 | GEO

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

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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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Project description:Members of the HMGN protein family bind to nucleosomes and affect chromatin structure and functions as transcription, replication and DNA repair as well as epigenetic modifications. Overexpression of Hmgn1 may be linked to the etiology of Down syndrome while underexpression may be linked to some leukemias. Hmgn3 is highly expressed in eye and in brain and might influence behavioral phenotype. For Hmgn5 effects on transcription levels e.g. in liver are suggested. Total RNA obtained from four homozygote mutant and wildtype male mice were compared.

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