Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tet1 is a tumor suppressor of hematopoietic maligancy [RRBS]

ABSTRACT: Loss of Tet1 expression causes global 5mC and 5hmC changes in stem and progenitor cells in mice and causes enhanced Pro-B cell self-renewal, increased DNA damage and B-lymphomageneis. In this study we performed reduced representative bisulfite sequencing (RRBS) of DNA from WT and Tet1 KO LSK cells. DNA methylation sequencing was performed and analyzed using an enhanced reduced representation (ERRBS) methodology as previously described. DNA was extracted from purified LSK cells of 6-month old WT and Tet1 KO mice, Bisulphite treatment was performed using the EZ DNA Methylation Kit (Zymo Research). Libraries were amplified according to illumina protocols and sequenced on an Illumina HiSeq2500 machine DNA methylation profiling of LSK cells in WT and Tet1 KO mice.

ORGANISM(S): Mus musculus

SUBMITTER: Luisa Cimmino

PROVIDER: E-GEOD-65919 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Tet1 is a tumor suppressor of hematopoietic maligancy [array]

Project description:Loss of Tet1 expression causes global 5mC and 5hmC changes in stem and progenitor cells in mice and causes enhanced Pro-B cell self-renewal, increased DNA damage and B-lymphomageneis. In this study we performed microarray analysis of total LSK cells from WT and Tet1 KO mice. These results revealed that genes regulated byTet1 in LSKs included Histones, DNA repair enzymes and B-lineage specific factors. LSK cells were purified from the bone marrow of 6-month old WT and Tet1 KO mice . RNA was extracted using RNeasy kit (Qiagen) and hybridized on Affymetrix microarrays. Microarray profiling of LSK cells in WT and Tet1 KO mice.

2015-04-12 | E-GEOD-65913 | biostudies-arrayexpress

DNA methylation in the colon of Dnmt3b-induced and control mice

Project description:The methylation status of colon epithelial cells was profiled in wild type mice and mice expressing a Dnmt3b transgene. Genome-scale methylation profiles were generated using reduced representation bisulfite sequencing (RRBS), with CpG methylation scored by promoter and also summarized by gene. Dnmt3b expression is associated with a strong increase in de novo methylation of a discrete subset of "methylation sensitive" genes which show a strong concordance with genes methylated in human colon cancer. These results, together with further analysis, indicate that colon epithelial cell methylation in the Dnmt3b mouse model predicts DNA methylation of human colon cancer with high confidence. Three each of Dnmt3b-induced and control mice, each split into two fractions.

2011-10-25 | E-GEOD-26758 | biostudies-arrayexpress

Dissection of TET1 catalytic and non-catalytic functions reveals DNA demethylation independent gene and ERV regulation

Project description:Surveillance of DNA methylation in mammals is critical for genome stability and epigenetic regulation. The discovery of the ten-eleven translocation (TET) proteins catalyzing the oxidation from 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC) revolutionized the understanding of DNA methylation dynamics. Interestingly, in recent years evidence accumulated that TET1 also harbours non-catalytic functions. However, the role and mechanism of TET1 DNA demethylation independent functions still remain poorly understood. Here, we use genome engineering and quantitative multi-omics approaches to dissect the non-catalytic role of TET1. Strikingly, we find that the majority of transcriptional regulation depends on non-catalytic functions of TET1. To gain insights into possible mechanisms by which TET1 regulates transcription independent of DNA demethylation, we asked if the loss of TET1 is accompanied by changes in the histone modificaiton landscape. To this end, we compared the relative abundances of core histone modifications between Tet1 KO, Tet1 CM and WT mESCs using quantitative LC-MS/MS analysis. Surprisingly, we observed a profound global reduction of pH4Kac and H4K20me3 as well as H3K27me3 in Tet1 KO mESC. Vice versa, the monomethylation states of the latter two residues, H3K27me1 and H4K20me1 were significantly increased in Tet1 KO. Similar to the results from the transcriptome data, most of these changes were specific to Tet1 KO cells.

2022-08-11 | PXD028566 | Pride

Tet1 is a tumor suppressor of hematopoietic maligancy [RRBS]

Project description:Loss of Tet1 expression causes global 5mC and 5hmC changes in stem and progenitor cells in mice and causes enhanced Pro-B cell self-renewal, increased DNA damage and B-lymphomageneis. In this study we performed reduced representative bisulfite sequencing (RRBS) of DNA from WT and Tet1 KO LSK cells.

2015-04-12 | GSE65919 | GEO

RNA Sequencing of H1 WT hESCs, H1 QSER1 KO hESCs, H1 TET1 KO hESCs, H1 QSER1/TET1 DKO hESCs, WT Day10 EBs, QSER1 KO Day10 EBs, TET1 KO Day10 EBs, QSER1/TET1 DKO Day10 EBs, WT PP1, QSER1 KO PP1, TET1 KO PP1, and QSER1/TET1 DKO PP1.

Project description:RNA Sequencing of H1 WT hESCs, H1 QSER1 KO hESCs, H1 TET1 KO hESCs, H1 QSER1/TET1 DKO hESCs, WT Day10 embryoid bodies (EBs), QSER1 KO Day10 EBs, TET1 KO Day10 EBs, QSER1/TET1 DKO Day10 EBs, WT pancreatic progenitors (PP1), QSER1 KO PP1, TET1 KO PP1, and QSER1/TET1 DKO PP1. DNA methylation is essential to mammalian development, and dysregulation can cause serious pathological conditions. Key enzymes responsible for deposition and removal of DNA methylation are known, but how they cooperate to tightly regulate the methylation landscape remains a central question. Utilizing a knockin DNA methylation reporter, we performed a genome-wide CRISPR/Cas screen in human embryonic stem cells to discover DNA methylation regulators. The top screen hit was an uncharacterized gene QSER1, which proved to be a key guardian of bivalent promoters and poised enhancers of developmental genes, especially those residing in DNA methylation valleys (or canyons). We further demonstrate cooperation of QSER1 and TET1 through genetic and biochemical interactions to inhibit DNMT3-mediated de novo methylation and safeguard developmental programs.

2021-03-19 | GSE169209 | GEO

Transcriptome profiling of wild type and Tet1-null primordial germ cells (PGC) by Bisulfite-seq

Project description:Purpose: To investigate the effect of Tet1 depletion on global DNA methylation, we performed whole-genome bisulfite sequencing (WGBS). Methods: Starting with as little as 1400-5251 manually micro-dissected PGCs, we used an ultra-low input method, Tn5mC-seq. Results: We generated 945 million reads for Tet1Gt/Gt PGCs and 302 million reads for wild-type PGCs. We obtained 14-16 million CpG sites per genotype at 1.76-2.66x genome coverage, which enables a comprehensive view of genome-wide DNA methylation patterns in E13.5 PGCs. PGCs are almost completely unmethylated genome-wide. Loss of Tet1 led to a subtle increase of methylation level in various genomic elements including promoters, exons, introns and repetitive elements in Tet1Gt/Gt PGCs (p<0.01). Local analysis identified 4,337 differentially methylated regions (DMRs) between Tet1-/- PGCs and wild-type cells. These DMRs are associated with 5,261 genes, among which 271 genes also exhibited differential gene expression and enriched for the cell cycle pathway (FDR=0.02). Conclusions: This result revealed that demethylation of certain set of cell cycle genes is largely abolished in the Tet1-/- PGCs. Genome-wide methylation profiles of primordial germ cells derived from the wild type (WT) and Tet1-null female embryos at E13.5 were generated by whole genome bisulfite sequencing using Illumina Hiseq.

2012-11-20 | E-GEOD-41912 | biostudies-arrayexpress

Tet1 is a tumor suppressor of hematopoietic maligancy [array]

2015-04-12 | GSE65913 | GEO

Pregnancy-associated alterations in DNA methylation patterns of mammary epithelial stem cells [mRRBS]

Project description:Mammary gland development and luminal differentiation occur largely postnatally during puberty and pregnancy. We found that pregnancy had the most significant effects on stem cells, inducing a distinct epigenetic state that remained stable through life. Mammary glands were collected from mice at non-pregnant and pregnant stages for DNA extraction and DNA methylation analysis via mRRBS (multiplexed reduced representation bisulfite sequencing).

2015-01-22 | E-GEOD-54149 | biostudies-arrayexpress

Transcriptional and epigenetic program changes of induced beta cells over time [RRBS-seq]

Project description:Direct lineage conversion is a promising approach to generate therapeutically important cell types for disease modeling and tissue repair. However, it is often unclear whether lineage-reprogrammed cells remain stable long-term and whether the properties of the reprogrammed cells evolve over time. Here, using an improved method of converting pancreatic acinar cells to beta-cells, we show that induced beta-cells persist in the adult pancreas for up to 14 months and form islet-like structures. Detailed analyses of induced cells over 7 months reveal that global DNA methylation changes occur rapidly whereas transcription network remodeling evolves over two months to resemble that of endogenous beta-cells and then stabilizes thereafter. Progressive gain of beta-cell function by converted cells during the 7 month period coincides with both transcriptional changes and the formation of islet-like structures. These studies demonstrate the ability of lineage-reprogrammed cells to achieve a stable state and identify key cellular and molecular milestones during their long-term evolution. Acinar cells and beta cells were collected as control, as well as induced beta cell samples at day 10, day 30, day 60, and 7 months

2014-11-15 | E-GEOD-59615 | biostudies-arrayexpress

Comparative analysis of Tet2 catalytic deficient and knockout bone marrow over time

Project description:In this study, we investigated the role of Tet2 in regulation of hematopoietic genes by performing transcriptomic analysis of Tet2 WT, Mut, and KO LSK and Lin– cells at 3, 6, 9, and 12 months by RNA-seq, and mapping the DNA methylation landscape of 3-month-old Tet2 WT, Mut, and KO LSK and Lin– cells. (1) We find that loss of Tet2 (Tet2 KO) vs. a loss of Tet2 catalytic function (Tet2 Mut) at different time points and cell types causes distinct gene expression changes when compared to WT samples as assessed by RNA-seq. (2) Additionally, we find that many genes implicated in lymphoma and leukemia are deregulated in Tet2 Mut and KO LSK and Lin– cells, consistent with the phenotypes observed in mice transplanted with Tet2 Mut and KO bone marrow. (3) We also mapped genome-wide DNA methylation levels of WT, Tet2 Mut, and KO LSK and Lin– cells at 3 months by WGBS and establish a role for Tet2 in demethylating genes implicated in lymphoma and leukemia initiation and progression.

2023-06-01 | GSE227977 | 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