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Genome-wide expression profiling analysis of a Hmgn1, 3 and 5 mutant mouse model

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE39062 | GEO | 2013/07/03

SECONDARY ACCESSION(S): PRJNA169857

REPOSITORIES: GEO

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Genome-wide expression profiling analysis of a Hmgn1, 3 and 5 mutant mouse model

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.

2013-07-03 | E-GEOD-39062 | biostudies-arrayexpress

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

Transcription profiling of mouse AtT20 pituitary gland cells following overexpression or down regulation of NSBP1

Project description:Chromatin architectural protein NSBP1/HMGN5 belongs to the family of HMGN proteins which specifically interact with nucleosomes via Nucleosome Binding Domain, unfold chromatin and affect transcription. Mouse NSBP1 is a new and uncharacterized member of HMGN protein family. NSBP1 is a nuclear protein which is localized to euchromatin, binds to linker histone H1 and unfolds chromatin. We analyzed the effect of altered expression levels of mouse NSBP1 protein on global gene expression profile in AtT20 pituitary cells. We found that NSBP1 modulates the fidelity of cellular transcription in the nucleosome binding-dependent manner. Experiment Overall Design: Stable clones overexpressing wild type mouse NSBP1 protein or mutated NSBP1SE protein which does not bind to nucleosomes were generated by retroviral infection of AtT20 cells. siRNA treatment was applied to down regulate NSBP1 in the cells. Total RNA was collected from biological triplicates and analyzed by Affymetrix expression arrays.

2009-06-23 | E-GEOD-16564 | biostudies-arrayexpress

Expression data from AtT20 mouse pituitary gland cells following overexpression or down regulation of NSBP1

2009-06-13 | GSE16564 | GEO

HMGN5, an RNA and Nucleosome binding protein required for chromatin de-condensation and gene activation [CLIP-seq]

Project description:HMGN5 is a member of the HMGN family that de-compacts chromatin and regulates gene expression. Chromatin-associated RNAs are known to play a major role in controlling gene expression and chromatin architecture. We recently showed that RNA is required to open chromatin structure in Drosophila. A potential involvement of RNA in the HMGN5-dependent opening of chromatin has not been studied so far. Here we revealed that HMGN5 has a novel and specific RNA binding activity, which is extended to the HMGN family. HMGN5 is associated preferentially with active regulatory regions and binds co-transcriptionally to the nascent RNA. Additionally, we showed that HMGN5 co-localizes and interacts with CTCF, which suggests a cooperative role of both proteins in organizing higher order structures of chromatin. We showed that HMGN5 forms mutually exclusive complexes with chromatin and RNA in vitro, altogether suggesting a dual role for HMGN5 in gene regulation, switching from nucleosome to RNA binding during gene activation.

2024-05-08 | GSE166101 | GEO

HMGN5, an RNA and Nucleosome binding protein required for chromatin de-condensation and gene activation [ChIP-seq]

2024-05-08 | GSE166098 | GEO

HMGN5, an RNA and Nucleosome binding protein required for chromatin de-condensation and gene activation [RNA-seq]

2024-05-08 | GSE166091 | GEO

HMGN5, an RNA and Nucleosome binding protein required for chromatin de-condensation and gene activation

Project description:The packaging of DNA into chromatin and its compaction within cells renders the underlying DNA template un-accessible for processes like transcription, replication and repair. Active mechanisms as chromatin modifying activities or the association with non-coding RNAs can de-condense chromatin, rendering it accessible for the DNA dependent processes. High mobility group proteins (HMG) are small architectural chromatin proteins that were shown to contribute to the regulation of chromatin accessibility and condensation. Here we show that HMGN5, a member of the HMGN family is capable to de-compact chromatin and to activate gene expression. We identified and characterized a novel RNA binding domain within HMGN5 that overlaps with its nucleosome binding domain (NBD). HMGN5 binds exclusively to nucleosomes or RNA, suggesting a switching mechanism and different functionalities depending on its binding partner. For this we show that HMGN5 is bound to regulatory regions of the genes that it tends to activate and also is found on the primary transcript of these genes. The results suggest that HMGN5 is switching from the chromatin binding to the RNA binding state after gene activation, potentially improving RNA synthesis. Furthermore, HMGN5 co-localizes and directly interacts with CTCF, suggesting a cooperative role of both proteins in organizing higher order structures of chromatin and active chromatin domains.

2024-05-08 | GSE166103 | GEO

Expression data from wild-type and HMGN1 knockout mice injected with N-nitrosodiethylamine

Project description:HMGN1 contributes to the shortened latency of liver tumorigenesis by changing a chromatin structure and expression of relevant genes To assess the molecular mechanisms underlying accelerated tumor development in Hmgn1-/- mice, we performed the gene expression profiling of liver cells at early stages Expression profiles has been compared between Hmgn1+/+ and Hmgn1-/- mice livers at 4 weeks after birth and at 12 weeks after DEN or saline (control) injection at 4 weeks

2013-08-24 | E-GEOD-44356 | biostudies-arrayexpress

Genomic Profiling of HMGN1 Reveals an Association with Chromatin at Regulatory Regions

Project description:High mobility group (HMG) proteins interact with other architectural proteins to regulate chromatin structure. We performed genome-wide mapping experiments to examine the distribution of HMGN1 across the human genome. We discovered that HMGN1 proteins are enriched at regulatory regions such as DNase I HS sites, distal transcription factor binding sites and promoters of actively transcribed genes. YY1, the Yin Yang 1 transcription factor, is a ubiquitous transcription factor that functions either as a transcriptional activator or a repressor, depending on its interacting partner. To test the preferential localization of HMGN1 with active regulatory regions, we examined the association of transcription factor YY1 and HMGN1 in CD4+ T cells. Examination of the genomic profile of HMGN1 and the relationship with regulatory elements in CD4+ T cells.

2010-11-30 | E-GEOD-25674 | biostudies-arrayexpress

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