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Active and repressed chromatin domains exhibit distinct nucleosome segregation during DNA replication

ABSTRACT: Active and repressed chromatin domains exhibit distinct nucleosome segregation during DNA replication

PROVIDER: PRJNA561753 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10017655.fastq.gz	Fastqsanger.gz
	SRR10017656.fastq.gz	Fastqsanger.gz
	SRR10017657.fastq.gz	Fastqsanger.gz
	SRR10017658.fastq.gz	Fastqsanger.gz
	SRR10017659.fastq.gz	Fastqsanger.gz

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Active and repressed chromatin domains exhibit distinct nucleosome segregation during DNA replication

Project description:Chromatin domains and their associated structures must be faithfully inherited through cellular division to maintain cellular identity. Yet, accessing the localized strategies preserving chromatin domain inheritance, specifically the transfer of parental, pre-existing nucleosomes with their associated post-translational modifications (PTMs) during DNA replication is challenging in living cells. We devised an inducible, proximity-dependent labeling system to irreversibly mark replication-dependent H3.1 and H3.2 histone-containing nucleosomes at single desired loci in mouse embryonic stem cells such that their fate after DNA replication could be followed. Strikingly, repressed chromatin domains are preserved through the local re-deposition of parental nucleosomes. In contrast, nucleosomes decorating active chromatin domains do not exhibit such preservation. Notably, altering cell fate leads to an adjustment in the positional inheritance of parental nucleosomes that reflects the corresponding changes in chromatin structure. These findings point to important mechanisms that contribute to parental nucleosome segregation to preserve cellular identity.

2019-10-31 | GSE136245 | GEO

Active and Repressed Chromatin Domains Exhibit Distinct Nucleosome Segregation during DNA Replication.

Project description:Chromatin domains and their associated structures must be faithfully inherited through cellular division to maintain cellular identity. However, accessing the localized strategies preserving chromatin domain inheritance, specifically the transfer of parental, pre-existing nucleosomes with their associated post-translational modifications (PTMs) during DNA replication, is challenging in living cells. We devised an inducible, proximity-dependent labeling system to irreversibly mark replication-dependent H3.1 and H3.2 histone-containing nucleosomes at desired loci in mouse embryonic stem cells so that their fate after DNA replication could be followed. Strikingly, repressed chromatin domains are preserved through local re-deposition of parental nucleosomes. In contrast, nucleosomes decorating active chromatin domains do not exhibit such preservation. Notably, altering cell fate leads to an adjustment of the positional inheritance of parental nucleosomes that reflects the corresponding changes in chromatin structure. These findings point to important mechanisms that contribute to parental nucleosome segregation to preserve cellular identity.

| S-EPMC6917041 | biostudies-literature

Inheritance of Repressed Chromatin Domains during S-phase Requires the Histone Chaperone NPM1

Project description:The epigenetic process safeguards cell identity during cell division through the inheritance of appropriate gene expression profiles. We demonstrated previously that parental nucleosomes are inherited by the same chromatin domains during DNA replication only in the case of repressed chromatin. We now show that this specificity is conveyed by NPM1, a histone H3/H4 chaperone. Proteomic analyses of late S-phase chromatin revealed NPM1 in association with both H3K27me3, an integral component of facultative heterochromatin and MCM2, an integral component of the DNA replication machinery; moreover NPM1 interacts directly with PRC2 and with MCM2. Given that NPM1 is essential, the inheritance of repressed chromatin domains was examined anew using mESCs expressing an auxin-degradable version of endogenous NPM1. Upon NPM1 degradation, cells accumulated in S-phase of the cell-cycle and parental nucleosome inheritance from repressed chromatin domains was markedly compromised. Appropriate inheritance required the NPM1 acidic patches that function in chaperone activity, pointing to NPM1 being integral to the epigenetic process.

2022-04-27 | GSE183090 | GEO

Inheritance of Repressed Chromatin Domains during S-phase Requires the Histone Chaperone NPM1

Project description:Inheritance of Repressed Chromatin Domains during S-phase Requires the Histone Chaperone NPM1

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Genome of mouse ES cells is organized as nucleosome wrapping domains

Project description:In this research, we investigated the wrapping length of DNA on nucleosomes across the whole genome using wrapping-seq. We discovered that the mouse genome chromatin forms nucleosome wrapping domains (NRDs). NRDs are conserved from flies to human cells. Additionally, our study found that the degree of nucleosome wrapping decreases and matures after DNA replication. Moreover, the degree of nucleosome wrapping is associated with the transcriptional status of genes. Furthermore, we observed that nucleosome unwrapping states delineate 3-D genome organization. In conclusion, our wrapping-seq analysis has revealed a novel higher-order chromatin organization.

2024-10-28 | GSE243091 | GEO

The modulation of CHD4 nucleosome remodelling activity by auxiliary domains suggests unifies mechanistic aspects of chromatin remodelling across enzyme families

Project description:We determine the impact of auxiliary domains on the nucleosome sliding activity of CHD4. This dataset comprises the crosslinking mass spectrometry data we reported.

2023-03-11 | PXD033633 | Pride

Structure of nucleosome-bound human PBAF complex

Project description:BAF and PBAF are mammalian SWI/SNF family chromatin remodeling complexes that possess multiple histone/DNA-binding subunits and create nucleosome-depleted/free regions for transcription activation. Despite previous structural studies and recent advance of SWI/SNF family complexes, it remains incompletely understood how PBAF-nucleosome complex is organized. Here we determined structure of 13-subunit human PBAF in complex with acetylated nucleosome in ADP-BeF3-bound state. Four PBAF-specific subunits work together with nine BAF/PBAF-shared subunits to generate PBAF-specific modular organization, distinct from that of BAF at various regions. PBAF-nucleosome structure reveals six histone-binding domains and four DNA-binding domains/modules, the majority of which directly bind histone/DNA. This multivalent nucleosome-binding pattern, not observed in previous studies, suggests that PBAF may integrate comprehensive chromatin information to target genomic loci for function. Our study reveals molecular organization of subunits and histone/DNA-binding domains/modules in PBAF-nucleosome complex and provides structural insights into PBAF-mediated nucleosome association complimentary to the recently reported PBAF-nucleosome structure.

2023-03-11 | PXD036708 | Pride

Genome of mouse ES cells is organized as nucleosome wrapping domains

Project description:Genome of mouse ES cells is organized as nucleosome wrapping domains

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Asymmetric Segregation of the Nucleosome Remodeling and Deacetylase Complex during Asymmetric Cell Divisions

Project description:Asymmetric Segregation of the Nucleosome Remodeling and Deacetylase Complex during Asymmetric Cell Divisions

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Asymmetric Segregation of the Nucleosome Remodeling and Deacetylase Complex during Asymmetric Cell Divisions

Project description:Asymmetric cell divisions (ACDs) generate two daughter cells with identical genetic information but distinct cell fates. Epigenetic mechanisms are crucial for cell fate specification, and it remains unclear how epigenetic information is inherited. Here, we report asymmetric segregation of the nucleosome remodeling and deacetylase complex (NuRD) during ACDs in Caenorhabditis elegans. NuRD is enriched to chromosomes of the future surviving but not apoptotic daughter cell, whereas NuRD evenly distributes to two viable siblings. Disruption of ACDs causes symmetric NuRD inheritance, and an ectopic gain of NuRD in apoptotic daughters allows cell survival and differentiation. Lack of NuRD upregulates the expression of the vital cell death-inducing gene egl-1 by increasing H3K27 acetylation on the egl-1 locus, which activates the EGL-1-CED-9-CED-4-CED-3 pathway to promote apoptosis. We propose that biased NuRD segregation during ACDs provides a previously unrecognized yet common mechanism for asymmetrically partitioning epigenetic information that contributes to binary cell fate decisions.

2022-12-30 | GSE167379 | GEO

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