Mus musculus strain:C57BL
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA305408 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2983930.fastq.gz | Fastqsanger.gz | |||
| SRR2983930_1.fastq.gz | Fastqsanger.gz | |||
| SRR2983930_2.fastq.gz | Fastqsanger.gz | |||
| SRR2985200.fastq.gz | Fastqsanger.gz | |||
| SRR2985200_1.fastq.gz | Fastqsanger.gz |
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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: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.
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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.
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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.
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Project description:HMGN (high mobility group N) is a family of intrinsically disordered nuclear proteins that binds to nucleosomes, alters the structure of chromatin and affects transcription. A major unresolved question is the extent of functional specificity, or redundancy, between the various members of the HMGN protein family. Here we analyze the transcriptional profile of cells in which the expression of various HMGN proteins has been either deleted or doubled. The results reveal an HMGN-variant specific effect on the fidelity of the cellular transcription profile, indicating that functionally, the various HMGN subtypes are not fully redundant. RNA was collected from either primary knock-out MEFs or SV40-transformed MEFs and MIN6 cells over expressing various HMGN proteins and mutants and hybridized to Affymetrix arrays. We obtained a double ammount of HMGN proteins in MEFs and MIN6 cells by retroviral infection and subsequent selection procedure. We collected all infected cells (pools, not clones) in order to eliminate the effect of viral integration in the genome.
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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.
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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 | GSE166098 | GEO
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.
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Project description:HMGN (high mobility group N) is a family of intrinsically disordered nuclear proteins that binds to nucleosomes, alters the structure of chromatin and affects transcription. A major unresolved question is the extent of functional specificity, or redundancy, between the various members of the HMGN protein family. Here we analyze the transcriptional profile of cells in which the expression of various HMGN proteins has been either deleted or doubled. The results reveal an HMGN-variant specific effect on the fidelity of the cellular transcription profile, indicating that functionally, the various HMGN subtypes are not fully redundant.
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