Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Reduced representative bisulfite sequencing (RRBS) analysis for a genome-wide comparison of DNA methylation in wild-type, USP7-KO-1, DNMT3A/3B-DKO and DNMT3A/DNMT3B/USP7-TKO HeLa cell lines.

ABSTRACT: Reduced representative bisulfite sequencing (RRBS) analysis for a genome-wide comparison of DNA methylation in wild-type, USP7-KO-1, DNMT3A/3B-DKO and DNMT3A/DNMT3B/USP7-TKO HeLa cell lines.

PROVIDER: PRJNA561408 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10011555_1.fastq.gz	Fastqsanger.gz
	SRR10011555_2.fastq.gz	Fastqsanger.gz
	SRR10011556_1.fastq.gz	Fastqsanger.gz
	SRR10011556_2.fastq.gz	Fastqsanger.gz
	SRR10011557_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Reduced representative bisulfite sequencing (RRBS) analysis for a genome-wide comparison of DNA methylation in wild-type, USP7-KO-1, DNMT3A/3B-DKO and DNMT3A/DNMT3B/USP7-TKO HeLa cell lines.

Project description:To better characterize the effects of USP7 on DNA methylation, we performed reduced representative bisulfite sequencing (RRBS) analysis for a genome-wide comparison of DNA methylation in wild-type, USP7-KO-1, DNMT3A/3B-DKO and DNMT3A/DNMT3B/USP7-TKO HeLa cell lines. RRBS analysis showed increased DNA methylation in USK7-KO cells and loss of USP7 elevates DNA methylation on pre-existing sites and de novo methylation.

2020-09-07 | GSE136159 | GEO

RNA-seq of triple knockout (TKO) mouse embryonic stem cells: Dnmt1-/-, Dnmt3a-/-, Dnmt3b-/-.

Project description:RNA-seq of triple knockout (TKO) mouse embryonic stem cells: Dnmt1-/-, Dnmt3a-/-, Dnmt3b-/-.

| PRJNA541006 | ENA

Active DNA Demethylation by DNMT3A and DNMT3B - Mechanistic Aspect and In Vivo Evidence

Project description:The DNA methylation program is at the bottom layer of the epigenetic regulatory cascade of vertebrate development. While the methylation at C-5 position of the cytosine (C) residues on the vertebrate genomes is achieved through the catalytic activities of the DNA methyltransferases (DNMTs), the conversion of the methylated cytosine (5mC) could be accomplished by the combined actions of the TET enzyme and DNA repair. Interestingly, it has been found recently that the mouse and human DNMTs also possess active DNA demethylation activity in vitro in a Ca2+- and redox condition-dependent manner. We report here the study of tracking down the fate of the methyl group removed from 5mC on DNA during in vitro demethylation reaction by mouse de novo DNMTs, i.e. DNMT3A and DNMT3B. Remarkably, the methyl group becomes covalently linked to the catalytic cysteines utilized by the two de novo DNMTs in their DNA methylation reactions. Thus, the forward and reverse reactions of DNA methylations by the DNMTs may utilize the same cysteine residue(s) as the active site despite of their distinctive pathways. Secondly, we demonstrate that active DNA demethylation of a heavily methylated GFP reporter plasmid by ectopically expressed DNMT3A or DNMT3B occurs in vivo in transfected human HEK 293 cells in culture. Furthermore, the extent of DNA demethylation by the DNMTs in this cell-based system is affected by Ca2+ homeostasis as well as by mutation of their putative active cysteines. These findings substantiate the roles of the vertebrate DNMTs as double-edged swords in DNA methylation-demethylation in vitro as well as in a cellular context.

2022-02-24 | PXD003401 | Pride

Expression data from mouse wild-type and Dnmt1-/-Dnmt3a-/-Dnmt3b-/- embryonic stem(ES) cells and nuclear transfer-trophoblastic stem(ntTS) cells, and wild-type trophoblastic stem(TS) cells, primitive endoderm cells, and extra-embryonic endoderm(XEN) cells

Project description:To investigate the role of DNA methylation in early embryogenesis, we created Dnmt1-/-Dnmt3a-/-Dnmt3b-/- triple knockout (TKO) embryos by the nuclear transfer (NT) technique using TKO ES cells as the nucleus donor, and found that the TKO NT embryos could develop into blastocysts. From the TKO NT blastocysts, we successfully established trophoblastic stem cells (ntTS cells), and these TKO ntTS cells could self-renew and contribute to the placenta in vivo. Expression profile analysis using microarray revealed that, although many genes were aberrantly expressed, the fundamental gene expression patterns of stem cells were retained in these TKO ntTS cells.

2010-09-03 | GSE20177 | GEO

Dnmt3a and Dnmt3b-mediated decommissioning of fetal enhancers linked to kidney disease

Project description:Cytosine methylation is an epigenetic mark that dictates cell fate and response to stimuli. The timing and establishment of methylation logic during kidney development remains unknown. DNA methyltransferase 3a and 3b are the enzymes capable of establishing de novo methylation. We generated mice with genetic deletion of Dnmt3a and Dnmt3b in nephron progenitor cells (Six2Cre Dnmt3a/3b) and kidney tubule cells (KspCre Dnmt3a/3b). We characterized KspCre Dnmt3a/3b mice at baseline and after injury. Unbiased omics profiling, such as whole genome bisulfite sequencing, reduced representation bisulfite sequencing and RNA sequencing were performed on whole-kidney samples and isolated renal tubule cells. KspCre Dnmt3a/3b mice showed no obvious morphologic and functional alterations at baseline. Knockout animals exhibited increased resistance to cisplatin-induced kidney injury, but not to folic acid–induced fibrosis. Whole-genome bisulfite sequencing indicated that Dnmt3a and Dnmt3b play an important role in methylation of gene regulatory regions that act as fetal-specific enhancers in the developing kidney but are decommissioned in the mature kidney. Loss of Dnmt3a and Dnmt3b resulted in failure to silence developmental genes. We also found that fetal-enhancer regions methylated by Dnmt3a and Dnmt3b were enriched for kidney disease genetic risk loci. Methylation patterns of kidneys from patients with CKD showed defects similar to those in mice with Dnmt3a and Dnmt3b deletion. Our results indicate a potential locus-specific convergence of genetic, epigenetic, and developmental elements in kidney disease development.

2020-03-03 | GSE134267 | GEO

RNA-seq of triple knockout (TKO) mouse embryonic stem cells: Dnmt1-/-, Dnmt3a-/-, Dnmt3b-/-.

Project description:TKO mouse embryonic stem cells were cultured in serum/LIF and 2i/LIF in order to investigate the role of methylation in the transcriptional regulation of ground state cells (Clone: TKO 121, Tsumura et.al. 2006).

2020-06-19 | GSE130686 | GEO

DNA methyltransferase 3B (DNMT3B) mutations in ICF syndrome: gene expression analysis

Project description:Genome-wide DNA methylation patterns are established and maintained by the coordinated action of three DNA methyltransferases, DNMT1, DNMT3A, and DNMT3B. DNMT3B hypomorphic germline mutations are responsible for two-thirds of Immunodeficiency, Centromere Instability, Facial Anomalies (ICF) syndrome cases. The molecular defects in transcription, DNA methylation, and chromatin structure in ICF cells remain relatively uncharacterized. We used expressing microarrays to define the global program of gene expression to elucidate the role of DNMT3B in these processes using EBV-immortalized lymphoblastoid cell lines (LCLs) derived from ICF syndrome and normal individuals. Keywords: disease-state analysis

2007-11-01 | GSE9499 | GEO

DNA methylation analysis and expression profiling during murine embryogenesis and in embryos deficient for DNMT3A or DNMT3B

Project description:We quantified the targets and kinetics of DNA methylation acquisition in mouse embryos, and determined the contribution of the de novo methyltransferases DNMT3A and DNMT3B to this process. We provide single-base maps of cytosine methylation by RRBS from the blastocysts to post-implantation stages and in embryos lacking DNMT3A or DNMT3B activity, and performed RNA-Seq in embryos lacking DNMT3B activity. We sequenced RRBS libraries prepared from genomic DNA isolated from embryos at consecutive stages of development between E3.5 and E11.5,and adult differentiated cells (sperm, liver). We performed RRBS on blastocysts at E3.5/E4.5, dissected epiblasts at E5.5/E6.5/E7/5, whole embryos at E8.5/E10.5 and limbs at E11.5. RRBS experiments in Dnmt3a-/- and Dnmt3b-/- embryos were performed in biological duplicates on individual embryos. We sequenced RNA-Seq libraries prepared from total RNAs of three WT and Dnmt3b-/- littermate embryos collected at E8.5.

2014-11-14 | E-GEOD-60334 | biostudies-arrayexpress

The binding sites of SMAD2/3, Dnmt3a and Dnmt3b in pluripotent mESC, EBs and ME when Smad4 is lost with or without Dnmt3b knockdown

Project description:To understand the genome wide binding profile of SMAD2/3 when SMAD4 is lost, Smad2/3 ChIPseq was performed in SMAD4 knockout (S4KO) mouse embryonic stem cells (mESC) or in S4KO embryonic bodies (EBs). To figure out the effect of Dnmt3b on SMAD2/3 binding ability in the absence of SMAD4, we further performed SMAD2/3 CUT&Tag in EBs of S4KO and S4KO with Dnmt3b konckdown, as well as in mesendoderm (ME) stage of WT and S4KO. The binding sites of Dnmt3a and Dnmt3b were explored by Dnmt3a or Dnmt3b ChIP-seq and Dnmt3b CUT&Tag in WT EBs and S4KO EBs. WT with Dnmt3b knockdown and S4KO with Dnmt3b knockdown were used to as a control for the Dnmt3b CUT&Tag. Besides, we inserted a 3xFlag-tag at the C-terminus of Dnmt3a or Dnmt3b and then carried out Flag CUT&Tag in EBs.

2024-10-21 | GSE240786 | GEO

Comprehensive structure-function characterization of DNMT3B and DNMT3A reveals distinctive de novo DNA methylation mechanisms

Project description:Mammalian DNA methylation patterns are established by two de novo DNA methyltransferases DNMT3A and DNMT3B, which exhibit both redundant and distinctive methylation activities. However, the related molecular basis remains undetermined. Through comprehensive structural, enzymology and cellular characterizations of DNMT3A and DNMT3B, here we uncovered distinct and interrelated modes-of-action underlying their CpG site and flanking sequence interaction. Strikingly, K777 of DNMT3B makes direct contacts with the DNA base at the +1 flank position of the cytosine methylation site, which contrasts with its counterpart in DNMT3A that forms base-specific contacts with the CpG site. Consequently, there is a divergent substrate and flanking sequence preference between DNMT3A and DNMT3B in vitro and in cells, thus providing an explanation for site-specific epigenomic alterations seen in ICF syndrome patients with DNMT3B mutations. Together, this study reveals crucial, yet complicated interplays of DNMT3s, DNA sequences and resultant methylation.

2020-06-18 | GSE145899 | GEO

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