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Chromatin restriction by the nucleosome remodeler Mi-2β and functional interplay with lineage-specific transcription regulators controls B cell differentiation

ABSTRACT: Chromatin restriction by the nucleosome remodeler Mi-2β and functional interplay with lineage-specific transcription regulators controls B cell differentiation

PROVIDER: PRJNA535487 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8956060.fastq.gz	Fastqsanger.gz
	SRR8956070.fastq.gz	Fastqsanger.gz
	SRR8956080.fastq.gz	Fastqsanger.gz
	SRR8956061.fastq.gz	Fastqsanger.gz
	SRR8956071.fastq.gz	Fastqsanger.gz

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Similar Datasets

Chromatin restriction by the nucleosome remodeler Mi-2β and functional interplay with lineage-specific transcription regulators controls B cell differentiation

Project description:Coordinated induction but also repression of genes is key to normal differentiation. Although the role of lineage-specific transcription regulators has been extensively studied, their functional integration with chromatin remodelers, one of the key enzymatic machineries that control chromatin accessibility, remains ill-defined. Here we investigate the role of Mi-2b, a SNF-2-like nucleosome remodeler and key component of the Nucleosome Remodeling Deacetylase (NuRD) complex in early B cells. Inactivation of Mi-2b arrested differentiation at the large pre-B cell stage and caused de-repression of cell adhesion and cell migration signaling factors by increasing chromatin access at poised enhancers and chromosome architectural elements. Mi-2b also supported IL-7R signaling, survival and proliferation by repressing negative effectors of this pathway. Importantly, over-expression of Bcl2, a mitochondrial pro-survival factor and target of IL-7R signaling, partly rescued the differentiation block caused by Mi-2b loss. Mi-2b stably associated with chromatin sites that harbor binding motifs for IKAROS and EBF1 and physically associated with these transcription factors both on and off chromatin. Notably, Mi-2b shared loss-of-function cellular and molecular phenotypes with IKAROS and EBF1 albeit in a distinct fashion. Thus the nucleosome remodeler Mi-2b promotes pre-B cell differentiation by providing repression capabilities to distinct lineage-specific transcription factor-based regulatory networks.

2019-05-15 | GSE130315 | GEO

The Mi-2 nucleosome remodeler and the Rpd3 histone deacetylase are involved in piRNA-guided heterochromatin formation

Project description:In eukaryotes, trimethylation of lysine 9 on histone H3 (H3K9) is associated with transcriptional silencing of transposable elements (TEs). In drosophila ovaries, this heterochromatic repressive mark is thought to be deposited by SetDB1 on TE genomic loci after the initial recognition of nascent transcripts by PIWI-interacting RNAs (piRNAs) loaded on the Piwi protein. Here, we show that the nucleosome remodeler Mi-2, in complex with its partner MEP-1, forms a subunit that is transiently associated, in a MEP-1 C-terminus-dependent manner, with known Piwi interactors, including a recently reported SUMO ligase Su(var)2-10. Together with the histone deacetylase Rpd3, this module is involved in the piRNA-dependent TE silencing, correlated with H3K9 deacetylation and trimethylation. Therefore. drosophila piRNA-mediated transcriptional silencing involves three epigenetic effectors, a remodeler, Mi-2, an eraser, Rpd3 and a writer, SetDB1, in addition to the Su(var)2-10 SUMO ligase.

2020-07-21 | PXD018749 | Pride

Chromatin restriction by the nucleosome remodeler Mi-2β and functional interplay with lineage-specific transcription regulators control B-cell differentiation.

Project description:Coordinated induction, but also repression, of genes are key to normal differentiation. Although the role of lineage-specific transcription regulators has been studied extensively, their functional integration with chromatin remodelers, one of the key enzymatic machineries that control chromatin accessibility, remains ill-defined. Here we investigate the role of Mi-2β, a SNF-2-like nucleosome remodeler and key component of the nucleosome remodeling and histone deacetylase (NuRD) complex in early B cells. Inactivation of Mi-2β arrested differentiation at the large pre-B-cell stage and caused derepression of cell adhesion and cell migration signaling factors by increasing chromatin access at poised enhancers and chromosome architectural elements. Mi-2β also supported IL-7R signaling, survival, and proliferation by repressing negative effectors of this pathway. Importantly, overexpression of Bcl2, a mitochondrial prosurvival gene and target of IL-7R signaling, partly rescued the differentiation block caused by Mi-2β loss. Mi-2β stably associated with chromatin sites that harbor binding motifs for IKAROS and EBF1 and physically associated with these transcription factors both on and off chromatin. Notably, Mi-2β shared loss-of-function cellular and molecular phenotypes with IKAROS and EBF1, albeit in a distinct fashion. Thus, the nucleosome remodeler Mi-2β promotes pre-B-cell differentiation by providing repression capabilities to distinct lineage-specific transcription factor-based regulatory networks.

| S-EPMC6601517 | biostudies-literature

The Mi-2 nucleosome remodeler and the Rpd3 histone deacetylase are involved in piRNA-guided heterochromatin formation

2020-04-10 | GSE141237 | GEO

Nucleosome recognition and DNA distortion by the Chd1 remodeler revealed at 2.6 Å resolution

Project description:Chromatin remodelers are ATP-dependent enzymes that reorganize nucleosomes within all eukaryotic genomes. The Chd1 remodeler specializes in shifting nucleosomes into evenly spaced arrays, a defining characteristic of chromatin in gene bodies that blocks spurious transcription initiation. Linked to some forms of autism and commonly mutated in prostate cancer, Chd1 is essential for maintaining pluripotency in stem cells. Here we report a complex of yeast Chd1 bound to a nucleosome in a nucleotide-free state, determined by cryo-electron microscopy (cryo-EM) to 2.6 Å resolution. The structure shows a bulge of the DNA tracking strand where the ATPase motor engages the nucleosome, consistent with an initial stage in DNA translocation. Unlike other remodeler-nucleosome complexes, nucleosomal DNA compensates for the remodeler-induced bulge with a bulge of the complementary DNA strand one helical turn downstream from the ATPase motor. Unexpectedly, the structure also reveals an N-terminal binding motif, called ChEx, which binds on the exit-side acidic patch of the nucleosome. The ChEx motif can displace a LANA-based peptide from the acidic patch, which suggests a means by which Chd1 remodelers may block competing chromatin remodelers from acting on the opposite side of the nucleosome.

2022-02-23 | PXD025287 | Pride

The Mi-2 nucleosome remodeler and the Rpd3 histone deacetylase are involved in piRNA-guided heterochromatin formation

Project description:The Mi-2 nucleosome remodeler and the Rpd3 histone deacetylase are involved in piRNA-guided heterochromatin formation

| PRJNA592901 | ENA

Architecture of the chromatin remodeler RSC and insights into its nucleosome engagement

Project description:Eukaryotic DNA is packaged into nucleosome arrays, which are repositioned by chromatin remodeling complexes to control DNA accessibility. The Saccharomyces cerevisiae RSC (Remodeling the Structure of Chromatin) complex, a member of the SWI/SNF chromatin remodeler family, plays critical roles in genome maintenance, transcription, and DNA repair. Here, we report cryo-electron microscopy (cryo-EM) and crosslinking mass spectrometry (CLMS) studies of yeast RSC complex and show that RSC is composed of a rigid tripartite core and two flexible lobes. The core structure is scaffolded by an asymmetric Rsc8 dimer and built with the evolutionarily conserved subunits Sfh1, Rsc6, Rsc9 and Sth1. The flexible ATPase lobe, composed of helicase subunit Sth1, Arp7, Arp9 and Rtt102, is anchored to this core by the N-terminus of Sth1. Our cryo-EM analysis of RSC bound to a nucleosome core particle shows that in addition to the expected nucleosome-Sth1 interactions, RSC engages histones and nucleosomal DNA through one arm of the core structure, composed of the Rsc8 SWIRM domains, Sfh1 and Npl6. Our findings provide structural insights into the conserved assembly process for all members of the SWI/SNF family of remodelers, and illustrate how RSC selects, engages, and remodels nucleosomes.

2020-05-27 | PXD019400 | Pride

Nucleosome density shapes kilobase-scale regulation by a mammalian chromatin remodeler

Project description:SAMOSA, a method previously developed in the Ramani Lab, was employed to reveal nucleosome patterns from remodeling reactions in vitro with the Imitation Switch (ISWI) ATP-Dependent Remodeler ATPase, SNF2h. SAMOSA was further employed to reveal single-molecule nucleosome patterns in vivo from SNF2h knockout and re-expression murine embryonic stem cells.

2023-08-03 | GSE197979 | GEO

Role of Itc1 subnit in ISW2 remodeler in nucleosome positioning and spacing in Saccharomyces cerevisiae

Project description:Role of Itc1 subnit in ISW2 remodeler in nucleosome positioning and spacing in Saccharomyces cerevisiae

2024-04-07 | GSE205956 | GEO

Opposing chromatin remodeler activities control initiation frequency and start site selection

Project description:Using an integrated analysis of chromatin remodeler binding in unperturbed cells and nucleosome displacement activity upon rapid remodeler depletion or degradation, we investigate the interplay between these enzymes and their functional consequences. We show that many promoters are acted upon by multiple remodelers that operate either cooperatively or in opposition to determine the precise location of the key transcription start site-associated +1 nucleosome. Functional assays indicate that +1 nucleosome positioning reflects a trade-off between maximizing RNA Polymerase II recruitment and minimizing transcription initiation at incorrect sites. Interestingly, in the absence of any remodeling activity +1 nucleosomes largely maintain their positions. Our results provide a detailed picture of fundamental mechanisms linking promoter nucleosome architecture to productive transcription initiation.

2019-01-01 | GSE115412 | GEO

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