Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nucleosome intermediate preference of SMARCAD1 chromatin remodeler, and the structural insights

ABSTRACT: Nucleosome intermediate preference of SMARCAD1 chromatin remodeler, and the structural insights

PROVIDER: PRJNA1033990 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26593125_1.fastq.gz	Fastqsanger.gz
	SRR26593125_2.fastq.gz	Fastqsanger.gz
	SRR26593126_1.fastq.gz	Fastqsanger.gz
	SRR26593126_2.fastq.gz	Fastqsanger.gz
	SRR26593127_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Nucleosome intermediate preference of SMARCAD1 chromatin remodeler, and the structural insights

Project description:Examination of the repositioning of nucleosome and hexasome-sized particles induced by the SMARCAD1 family proteins in cells support the hexasome-binding mode. Our findings reveal a new mode of chromatin regulation, wherein the nucleosome intermediates are specially remodeled through an ATP-dependent process.

2024-11-01 | GSE246619 | GEO

ChIP-Seq of chromatin remodeler SMARCAD1 and H3K9me3 in female mouse embryonic stem cells (PGK12.1 XX)

Project description:Investigation of the co-occurance of the ATP-dependent chromatin remodeler SMARCAD1 and the histone modification H3K9me3 in the genome of PGK12.1 XX ES cells. ChIP-seq of endogenous SMARCAD1 was carried out in control and SMARCAD1-knockdown ES cells using a double crosslinking procedure. Additionally, H3K9me3 ChIP-seq was performed in double-cross linked control PGK12.1 XX cells. Input samples and precipitates with an IgG antibody were sequenced (Illumina HiSeq1500) as controls. Antibodies used were SMARCAD1 PAB15737 (Abnova) and H3K9me3 ab8898 (abcam).

2019-02-17 | E-MTAB-7012 | biostudies-arrayexpress

ChIP-Seq of SMARCAD1 and KAP1 in male mouse embryonic stem cells (E14)

Project description:The ATP dependent chromatin remodeler SMARCAD1 and the co-repressor KAP1 (Trim28/Tif1 beta) interact directly. We wanted to understand the interplay between these two proteins in the context of chromatin; in particular at repetitive sequences. Therefore, we carried out an investigation in E14 ES cells of the genome wide binding behaviour of KAP1 and FLAG-tagged SMARCAD1; both wild-type SMARCAD1 and a catalytically inactive mutant. The E14 cells analysed were either wild-type or depleted for endogenous SMARCAD1 protein. FLAG and KAP1 ChIP was performed on double-cross linked chromatin and sequenced on an Illumina HiSeq1500 with matched input controls. A FLAG antibody precipitation was carried out on cells not expressing FLAG tagged protein as an additional control.

2019-02-17 | E-MTAB-7011 | biostudies-arrayexpress

SMARCAD1 Regulates Nucleosome Positioning and Maintenance of the Naïve Pluripotent State

Project description:Genome-wide maps of nucleosome positioning in mouse ES cells with control shRNA and on Smarcad1 KD. MNase-seq data for human colo829 cells are also included.

2014-12-30 | GSE47802 | GEO

High-throughput sequence data of ChIP performed with anti-SMARCAD1 (ASNA) or anti-CBP actibodies.

Project description:Histone acetylation and nucleosome remodeling play a pivotal role in transcriptional regulation. While histone acetylase and ATP-dependent chromatin remodeling activities have been well characterized, how the two activities are coordinated remains to be uncovered. We discovered ATP-dependent histone H2A acetylation activity in Drosophila nuclear extracts. This activity was column-purified and demonstrated to be composed of CBP and SMARCAD1, which belongs to the Etl1 subfamily of the Snf2 family of helicase-related proteins. SMARCAD1 enhanced acetylation of H2A K5 and K8 by CBP in nucleosomes in an ATP-dependent fashion. Expression array analysis of S2 cells having ectopically expressed SMARCAD1 revealed up-regulated genes. Using native genome templates of these up-regulated genes, we found that SMARCAD1 activates their transcription in vitro. Knockdown analysis of SMARCAD1 and CBP indicated overlapping gene control, and ChIP-seq analysis of these commonly controlled genes showed that CBP is recruited to the promoter prior to SMARCAD1. Moreover, Drosophila genetic experiments demonstrated interaction between SMARCAD1/Etl1 and CBP/nej during development. The interplay between the remodeling activity of SMARCAD1 and histone acetylation by CBP sheds light on chromatin and the genome-integrity network. Examination of 2 different protein in 1 cell type.

2016-03-17 | E-GEOD-72666 | biostudies-arrayexpress

Role of SMARCAD1 and H3R26Cit in Maintenance of the Naïve Pluripotent State

Project description:Genome-wide maps of SMARCAD1 binding and histone modification H3R26Cit in mouse ES cells, histone modification H3K9me3, H3K4me3, H3K27Ac in Smarcad1 KD mouse ES cells, and histone modification H3K9me3 in mouse ES cells after PADI inhibition. Together with RNA-seq data for mouse ICM, blastocyst, embryonic stem cells and Smarcad1 KD cells.

2017-04-10 | GSE45338 | GEO

Histone H3.3 fills gaps in heterochromatin generated by Smarcad1 in mouse embryonic stem cells (ESC)

Project description:Nucleosome turnover concomitant with incorporation of the replication-independent histone variant H3.3 is a hallmark of regulatory regions in the animal genome. In our current understanding, nucleosome turnover is universally linked to DNA accessibility and histone acetylation. In mouse embryonic stem cells, H3.3 is also highly enriched at interstitial heterochromatin, most prominently intracisternal-A particle endogenous retroviral elements. Interstitial heterochromatin is established over confined domains by the TRIM28/SETDB1 corepressor complex and has stereotypical features of repressive chromatin, such as H3K9me3 and recruitment of all HP1 isoforms. Here, we demonstrate that fast histone turnover and H3.3 incorporation is compatible with these hallmarks of heterochromatin. We identify Smarcad1 to be a chromatin remodeler that generates nucleosome-free regions which are subsequently filled with histone H3.3, generating a surprisingly dynamic heterochromatin state. Loss of histone H3.3 elicits a highly specific opening of interstitial heterochromatin demonstrating that in the wake of Smarcad1 remodeling, H3.3 is required to maintain minimal DNA accessibility by reassembling nucleosomes.

2020-08-28 | GSE149080 | GEO

ChIP-Seq of chromatin remodeler SMARCAD1 and H3K9me3 in female mouse embryonic stem cells (PGK12.1 XX)

Project description:ChIP-Seq of chromatin remodeler SMARCAD1 and H3K9me3 in female mouse embryonic stem cells (PGK12.1 XX)

| PRJEB27790 | ENA

High-throughput sequence data of ChIP performed with anti-SMARCAD1 (ASNA) or anti-CBP actibodies.

2016-03-17 | GSE72666 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data