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A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina

ABSTRACT: A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina

PROVIDER: PRJNA151779 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR413416.fastq.gz	Fastqsanger.gz
	SRR413417.fastq.gz	Fastqsanger.gz
	SRR413418.fastq.gz	Fastqsanger.gz
	SRR413419.fastq.gz	Fastqsanger.gz
	SRR413420.fastq.gz	Fastqsanger.gz

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A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina

Project description:This SuperSeries is composed of the following subset Series: GSE35777: A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina [Tiling Array] GSE36048: A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina [ChIP-seq] Refer to individual Series

2012-02-24 | E-GEOD-36049 | biostudies-arrayexpress

A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina [ChIP-seq]

Project description:A large fraction of the mammalian genome is organized into inactive chromosomal domains associated with the nuclear lamina. Using genomic repositioning assays we show that Lamina associated domains (LADs), spanning the developmentally regulated IgH and Cyp3a loci, contain transportable DNA regions that associate chromatin with the nuclear lamina and repress gene activity in fibroblasts. We characterized DNA regions within LADs that are functionally capable of positioning chromatin domains at the inner nuclear membrane (INM) lamina. We mapped and characterized the IgH and other LADs in murine fibroblasts. We show that these murine LADs have a unique chromatin structure with discrete boundaries. We demonstrate DNA regions within LADs that are capable of directing the association of chromatin domains with the INM-lamina as well as the silencing of a co-integrated reporter gene.

2012-02-24 | E-GEOD-36048 | biostudies-arrayexpress

A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina [ChIP-seq]

2012-02-24 | GSE36048 | GEO

Spatial Compartmentalization at the Nuclear Periphery Characterized by Genome-wide Mapping

Project description:How gene positioning to the nuclear periphery regulates transcription remains largely unclear. We have previously observed the differential compartmentalization of transcription factors and histone modifications at the nuclear periphery in mouse C2C12 myoblasts. Here, we have integrated high throughput DNA sequencing into the DNA adenine methyltransferase identification (DamID) assay, and have identified ~15, 000 sequencing-based Lamina-Associated Domains (sLADs) in mouse 3T3 fibroblasts and C2C12 myoblasts. These genomic regions range from a few kb to over 1 Mb and cover ~30% of the genome, and are spatially proximal to the nuclear lamina (NL). Active histone modifications such as H3K4me2, H3K9Ac, H3K36me3 and H3K79me2 are all localized away from the nuclear periphery microscopically, and distributed predominantly out of sLADs genome-wide. Therefore, the spatial compartmentalization of active histone modifications likely characterizes a major portion of chromatin at the nuclear periphery in mammalian cells. Genomic regions around transcription start sites of expressed sLAD genes display reduced associations with the NL and possess active histone modifications; in contrast, gene bodies of expressed sLAD genes possess very low levels of active histone modifications. Our genome-wide analyses of NL-associated chromatin have enabled functional and mechanistic dissections of gene positioning on transcription regulation. generate DamID maps of genome-NL interaction for mouse 3T3 fibroblasts and C2C12 myoblasts

2013-10-30 | E-GEOD-41583 | biostudies-arrayexpress

Mapping the micro-proteome of the nuclear lamina and lamin associated domains

Project description:The nuclear lamina is a proteinaceous network of filaments that provide both structural and gene regulatory functions by tethering proteins and large domains of DNA, so-called lamin associated domains (LADs), to the periphery of the nucleus. LADs are a large fraction of the mammalian genome that are repressed, in part, by their association to the nuclear periphery. The genesis and maintenance of LADs is poorly understood as are the proteins that participate in these functions. In an effort to identify proteins that reside at the nuclear periphery and potentially interact with LADs, we have taken a two-pronged approach. First, we have undertaken an interactome analysis of the inner nuclear membrane bound LAP2β to further characterize the nuclear lamina proteome. To accomplish this, we have leveraged the BioID system, which previously has been successfully used to characterize the nuclear lamina proteome. Second, we have established a system to identify proteins that bind to LADs by developing a chromatin directed BioID system. We combined the BioID system with the m6A-tracer system which binds to LADs in live cells to identify LAD proximal and nuclear lamina proteins. In combining these datasets, we have further characterized the protein network at the nuclear lamina as well as identified putative LAD proximal proteins. Our analysis identifies many heterochromatin related proteins related to H3K9 methylation processes as well as many proteins related to cell cycle regulation identifying important proteins essential for LAD function.

2021-03-09 | PXD012943 | Pride

A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-02-24 | GSE36049 | GEO

A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina [Tiling Array]

Project description:These are the tiling array data for the experiments describing LADs on murine chromosomes 5, 12, and 15 by Dam-ID, as determined by LMNB and EMD Dam tagging and detection experiments Supplemental Bed file contains GADA algorithm calls for genomic regions of chromosomes 5, 12 and 15 (-1= no lad, high confidence, 0=indeterminate, 1=LAD, high confidence)

2012-02-14 | GSE35777 | GEO

Differential contributions of nuclear lamina association and genome compartmentalization to gene regulation

Project description:Purpose: A systematic analysis of how lamina association of chromosome regions influences their gene regulation in response to stimuli. Here, Lamin associated domains (LADs) of prostate cancer cell lines LNCaP and VCaP were experimentally measured using Lamin B1 ChIP-Seq so that these could be compared to previously published expression data in these cell lines and published LAD data from other cell types.

2022-09-12 | GSE213032 | GEO

Xist recruits the X chromosome to the nuclear lamina to enable chromosome-wide silencing

Project description:Xist orchestrates X chromosome inactivation, a process that entails chromosome-wide silencing and remodeling of the 3-dimensional structure of the X chromosome. Yet, it remains unclear whether these changes in nuclear structure are mediated by Xist and whether they are required for silencing. Here we show that Xist directly interacts with the Lamin B Receptor (LBR), an integral component of the nuclear lamina, and that this interaction is required for Xist-mediated silencing. We show that this interaction recruits the inactive X to the nuclear lamina and by doing so enables Xist to spread to actively transcribed genes across the X. Our results demonstrate that lamina recruitment changes the accessibility of DNA thereby enabling Xist, and its silencing proteins, to spread across the X to silence transcription. We examined the genomic localization of the Xist lncRNA using RNA Antisense Purification (RAP) in male mouse ES cells where the endogenous Xist promoter is replaced by a tet-inducible one (pSM33) containing 1) wild-type Xist (WT), 2) A-repeat deletion Xist (dA), 3) LBR binding site deletion Xist (dLBS), 4) dLBS-Xist rescued with LMNB1 (LMNB1Res), 5) LBR CRISPRi knock down (LBRKD), or 6) SHARP CRISPRi knock down (SHARPKD).

2016-07-24 | E-GEOD-80510 | biostudies-arrayexpress

Genome-wide maps of nuclear lamina interactions in AML12 cells upon G9a/GLP inhibition [DamID]

Project description:In differentiated cells, inhibition of methyltransferases G9a and GLP eliminated H3K9me2 predominantly at A-type genomic compartments, and the remaining H3K9me2 marks were strongly associated with B-type compartments and lamina-associated domains (LADs). However, inhibition of G9a/GLP in mouse embryonic stem cells (ESCs) removed most of the H3K9me2 modifications in both A and B compartments. Furthermore, chemical inhibition of G9a/GLP in mouse hepatocytes decreased chromatin-nuclear lamina (NL) interactions, increased the degree of genomic compartmentalization and the boundary strength of topologically associating domains (TADs) between A and B compartments, and altered the expression of hundreds of genes that were associated with alterations of chromatin structure.

2021-06-20 | GSE132957 | GEO

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