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Calcium Signaling Prompts NIPBL Recruitment at Active Enhancers and Promoters via Distinct Mechanisms to Reconstruct Genome Compartmentalization

ABSTRACT: Calcium Signaling Prompts NIPBL Recruitment at Active Enhancers and Promoters via Distinct Mechanisms to Reconstruct Genome Compartmentalization

PROVIDER: PRJNA644932 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12179300_1.fastq.gz	Fastqsanger.gz
	SRR12179300_2.fastq.gz	Fastqsanger.gz
	SRR12179400.fastq.gz	Fastqsanger.gz
	SRR12179301_1.fastq.gz	Fastqsanger.gz
	SRR12179301_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Calcium Signaling Prompts NIPBL Recruitment at Active Enhancers and Promoters via Distinct Mechanisms to Reconstruct Genome Compartmentalization

Project description:During developmental progression the genomes of immune cells undergo large-scale changes in chromatin folding. However, insights into the signals and epigenetics that induce alterations in nuclear architecture remain rudimentary. Here, we found that calcium influx rapidly recruited the cohesin-loading factor NIPBL to thousands of binding sites to dictate widespread changes in compartment segregation. The induction of NIPBL-binding was coordinate with increased P300, BRG1 and RNA Polymerase II co-occupancy, via different kinetics at active enhancers and promoters. Through acute degradation system, we found that enhancers, rather than promoters, are dependent on BAF complexes to induce NIPBL recruitment. Finally, we found that calcium signaling acts universally to orchestrate rapid redistribution of NIPBL in both primary innate and adaptive immune cells. Collectively, these data reveal how calcium signaling regulates NIPBL occupancy to orchestrate nuclear architecture.

2020-10-10 | GSE154051 | GEO

Calcium signaling instructs NIPBL recruitment at active enhancers and promoters via distinct mechanisms to reconstruct genome compartmentalization.

Project description:During developmental progression the genomes of immune cells undergo large-scale changes in chromatin folding. However, insights into signaling pathways and epigenetic control of nuclear architecture remain rudimentary. Here, we found that in activated neutrophils calcium influx rapidly recruited the cohesin-loading factor NIPBL to thousands of active enhancers and promoters to dictate widespread changes in compartment segregation. NIPBL recruitment to enhancers and promoters occurred with distinct kinetics. The induction of NIPBL-binding was coordinate with increased P300, BRG1 and RNA polymerase II occupancy. NIPBL-bound enhancers were associated with NFAT, PU.1, and CEBP cis elements, whereas NIPBL-bound promoters were enriched for GC-rich DNA sequences. Using an acute degradation system, we found that the histone acetyltransferases P300 and CBP maintained H3K27ac abundance and facilitated NIPBL occupancy at enhancers and that active transcriptional elongation is essential to maintain H3K27ac abundance. Chromatin remodelers, containing either of the mutually exclusive BRG1 and BRM ATPases, promoted NIPBL recruitment at active enhancers. Conversely, at active promoters, depletion of BRG1 and BRM showed minimal effect on NIPBL occupancy. Finally, we found that calcium signaling in both primary innate and adaptive immune cells swiftly induced NIPBL occupancy. Collectively, these data reveal how transcriptional regulators, histone acetyltransferases, chromatin remodelers, and transcription elongation promote NIPBL occupancy at active enhancers while the induction of NIPLB occupancy at promoters is primarily associated with GC-rich DNA sequences.

| S-EPMC7778268 | biostudies-literature

MAU2 and NIPBL variants in Cornelia de Lange syndrome reveal MAU2-independent loading of cohesin and uncover protective mechanisms against early truncating mutations in NIPBL

Project description:For its association with chromatin, the cohesin complex depends on a heterodimer formed by NIPBL and MAU2. Variants in NIPBL are the main cause of CdLS and result in NIPBL haploinsufficiency. Using CRISPR, we generated cells homozygous for an out-of-frame duplication in NIPBL. Remarkably, alternative translation initiation rescued NIPBL expression in these cells and produced an N-terminally truncated NIPBL that lacks MAU2-interaction domain, causing a dramatic reduction of MAU2 protein levels while a lot of NIPBL functions remain intact.

2020-06-10 | GSE122299 | GEO

RNA-seq of primary dissociated cortical Nipbl+/- neurons

Project description:RNA-seq of total RNA from Nipbl+/+ and Nipbl+/- dissociated cortical neurons at Day In Vitro (DIV10)

2021-02-28 | GSE161796 | GEO

ChIP-Seq for NIPBL for SMC1 in human lymphoblastoid cells (hLCLs)

Project description:The gene expression program is regulated by a cell-type specific chromosome architecture. The connection between enhancer and promoter regions is dependent on a protein complex containing Nipbl, Mediator and Cohesin. To gain insights into the chromosome architecture of human differentiated cells, we profiled NIPBL and SMC1 in lymphoblastoid cells (LCLs). DNA was enriched from hLCLs and chromatin immunoprecipitations (ChIPs) were analyzed by Solexa sequencing. ChIPs were performed using an antibody against NIPBL and SMC1. Whole cell extract is provided for background.

2012-06-01 | E-GEOD-38395 | biostudies-arrayexpress

Gene expression changes in limb buds of Nipbl-haploinsufficient mice

Project description:Multiple genes are dysregulated in hindlimb buds of Nipbl-deficient embryos. In all, more than 1000 limb bud genes were found to be significantly altered in expression by microarray analysis of E10.5 mouse hindlimb buds. Small changes in expression (mostly decreases) were observed for genes involved in FGF, BMP, and SHH pathways, as well as numerous genes involved in the Wnt/planar cell polarity signaling pathway. Genes involved in the Mediator complex, Cohesin function, and Hox gene expression and functions were also dysregulated in Nipbl deficient limb buds. Microarray analysis using RNA extracted from E10.5 hindlimb limb buds harvested from stage-matched Nipbl+/- (n=12) and wildtype (n=12)

2014-08-30 | E-GEOD-60932 | biostudies-arrayexpress

Genome occupancy of NIPBL in mouse P19 teratocarcinoma cells.

2020-01-01 | GSE132784 | GEO

Transcriptome analysis upon Nipbl, Brd2 and Brd4 knockdown in P19 cells

Project description:Mutations in NIPBL are the major cause of Cornelia de Lange Syndrome (CdLS). NIPBL is the cohesin loading factor and has recently been associated with the BET (Bromodomains and Extra Terminal (ET) domain) proteins BRD2 and BRD4. Related to this, a CdLS-like phenotype has been described associated to BRD4 mutations. To understand the relationship between NIPBL and BET proteins, we have performed RNA-Seq expression analysis following depletion of the different proteins in mouse P19 teratocarcinoma cells. Results indicate that genes regulated by NIPBL largely overlap with those regulated by BRD4 but not with those regulated by BRD2.

2020-01-01 | GSE132785 | GEO

Decreasing Wapl dosage partially corrects transcriptome phenotypes in Nipbl-/+ embryonic mouse brain

Project description:Cohesin rings interact with DNA and modulate expression of thousands of genes. NIPBL loads cohesin onto chromosomes and WAPL takes it off. Heterozygous mutations in NIPBL lead to a developmental disorder called Cornelia de Lange syndrome. Nipbl heterozygous mice are a good model for this disease. Mutations in WAPL were not known to cause disease or gene expression changes in mammals. Here we show dysregulation of >1000 genes in Wapl-/+embryonic mouse brains. The patterns of dysregulation are highly similar in Wapl and Nipbl heterozygotes, suggesting that Wapl mutations may cause disease in humans. Since WAPL and NIPBL have opposite effects on cohesin’s association with DNA, we asked whether a heterozygous Wapl mutation could correct phenotypes seen in Nipbl heterozygous mice. In fact, both gene expression and embryonic growth are partially corrected. Our data are consistent with the view that cohesin dynamics play a key role in regulating gene expression.

2022-10-11 | GSE203014 | GEO

Gastrulation-stage gene expression in Nipbl+/- mouse embryos foreshadows the development of syndromic birth defects

Project description:In animal models, Nipbl-deficiency phenocopies gene expression changes and birth defects seen in Cornelia de Lange Syndrome (CdLS), the most common cause of which is Nipbl-haploinsufficiency. Previous studies in Nipbl+/- mice identified aberrant gene expression and heart defects as early as cardiac crescent (CC) stage. Here, we performed single-cell RNA-sequencing on wildtype (WT) and Nipbl+/- mouse embryos at CC- and earlier (gastrulation) stages. Nipbl+/- embryos had fewer mesoderm cells than WT and altered proportions of mesodermal cell subpopulations. These findings were associated with an underexpression of genes implicated in driving specific mesodermal lineages. Nipbl+/- embryos also misexpressed developmentally-critical genes, including the transcription factor, Nanog, and genes governing left-right and anterior-posterior patterning. These events of cell misallocation and transcriptional dysregulation foreshadowed defects in tissue composition and patterning that arise later in Nipbl+/- mice, offering insights into early developmental contributions to birth defects in CdLS.

2023-05-07 | GSE151589 | GEO

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