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Functional genomic analysis of WT, Tet1-/-, Tet2-/-, Tet1-/-:Tet2-/- (DKO) murine embryonic stem cells

ABSTRACT: Functional genomic analysis of WT, Tet1-/-, Tet2-/-, Tet1-/-:Tet2-/- (DKO) murine embryonic stem cells

PROVIDER: PRJNA506422 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7797030_1.fastq.gz	Fastqsanger.gz
	SRR7797030_2.fastq.gz	Fastqsanger.gz
	SRR7797040_1.fastq.gz	Fastqsanger.gz
	SRR7797040_2.fastq.gz	Fastqsanger.gz
	SRR7797031_1.fastq.gz	Fastqsanger.gz

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RNA-seq of WT, Tet1-/-, Tet2-/-, Tet1-/-:Tet2-/- (DKO), and Tet1-/-:Tet2-/-:Tet3-/- (TKO) murine embryonic stem cells following six days of LIF withdrawal.

Project description:RNA-seq of WT, Tet1-/-, Tet2-/-, Tet1-/-:Tet2-/- (DKO), and Tet1-/-:Tet2-/-:Tet3-/- (TKO) murine embryonic stem cells following six days of LIF withdrawal.

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Project description:Reduced representation bisulfite sequencing (RRBS) of WT, Tet1-/-, Tet2-/-, Tet1-/-:Tet2-/- (DKO), and Tet1-/-:Tet2-/-:Tet3-/- (TKO) murine embryonic stem under normal culture conditions.

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Combined loss of Tet1 and Tet2 promotes B-cell, but not myeloid malignancies in mice

Project description:TET1/2/3 are methylcytosine dioxygenases regulating cytosine hydroxymethylation in the genome. Tet1 and Tet2 are abundantly expressed in HSC/HPCs and implicated in the pathogenesis of hematological malignancies. Tet2-deletion in mice causes myeloid malignancies, while Tet1-null mice develop B-cell lymphoma after an extended period of latency. Interestingly, TET1 and TET2 were often concomitantly down-regulated in acute B-lymphocytic leukemia. Here, we investigated the overlapping and non-redundant functions of Tet1/Tet2 in HSC maintenance and development of hematological malignancies using Tet1/2 double knockout (DKO) mice. DKO and Tet2-/- HSC/HPCs had overlapping and unique 5hmC and 5mC profiles and behaved differently. DKO mice exhibited strikingly decreased incidence and delayed onset of myeloid malignancies compared to Tet2-/- mice and in contrast developed lethal B-cell malignancies. Transcriptome analysis of DKO tumors revealed expression changes in many genes dysregulated in human B-cell malignancies, such as LMO2, BCL6 and MYC. These results highlight the critical roles of TET1 or TET2 individually and their cross-talks in the pathogenesis of hematological malignancies. Given the role of Tet proteins in 5mC oxidation, we employed a previously established chemical labeling and affinity purification method coupled with high-throughput sequencing (hMe-Seal) to profile the genome-wide distribution of 5hmC, as well as methylated DNA immunoprecipitation (MeDIP) coupled with high-throughput sequencing (MeDIP-seq) to profile 5mC using BM LK cells purified from young WT, Tet2-/- and DKO mice (6-10 wks old).

2015-11-12 | E-GEOD-73611 | biostudies-arrayexpress

Combined deficiency of Tet1 and Tet2 is compatible with development but leads to epigenetic instability

Project description:Tet enzymes (Tet1/2/3) convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). Tet1 and Tet2 mediate 5hmC generation in mouse embryonic stem cells (ESCs) and various embryonic and adult tissues. To investigate the effects of combined deficiency of Tet1 and Tet2 on pluripotency and development, we have generated Tet1 and Tet2 double knockout (DKO) ESCs and mice. DKO ESCs were depleted of 5hmC, but remained pluripotent with subtle defects in differentiation and changes in gene expression. Double mutant embryos and chimeras exhibited mid-gestation defects and postnatal DKO mice displayed partially penetrant neonatal lethality and stochastic perturbation of imprinting. Viable DKO animals developed normally to adulthood but had reduced 5hmC level, increased 5mC level and lacked 5hmC in germ cells. Nevertheless, DKO mice of both sexes were fertile with females having smaller ovaries and reduced fertility. Our data suggest that both Tet1 and Tet2 contribute to 5hmC levels during development. Their combined loss does not block differentiation and embryogenesis, but leads to partially penetrant embryonic and perinatal abnormalities and compromised viability. Moreover, the presence of substantial levels of 5hmC in DKO embryos and adult mice suggests a significant contribution of Tet3 in hydroxylation of 5mC during development. Methylation patterns in tissue samples from a series of wt and Tet1/Tet2 DKO embryos, neonates and adults were generated using methylated DNA immunoprecipitation with antibodies against 5mC (MeDIP) and 5hmC (hMeDIP) followed by deep sequencing.

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Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation [Bisulfite-Seq]

Project description:This study uses whole methylome sequencing to characterize the methylomes of mouse embryonic fibroblasts (MEF's). Two conditions were analyzed, MEF cells with intact TET1/TET2 enzymes (WT) and MEF cells with TET1/TET2 knocked out (DKO). Our results identify sets of differentially methylated genes which are correlated with TET1/TET2 induced expression changes of the corresponding genes. Whole methylome analysis of M. musculus MEF cells. Two conditions were sequenced and analyzed, the first is wild type (WT), the second (DKO) corresponds to knock-out of TET1 and TET2 enzymes.

2015-12-07 | E-GEOD-58610 | biostudies-arrayexpress

Combined loss of Tet1 and Tet2 promotes B-cell, but not myeloid malignancies in mice

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Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation [RNA-Seq]

Project description:This study uses whole-transcriptome sequencing to characterize the transcriptomes of mouse embryonic fibroblasts (MEF's). Two conditions were analyzed, MEF cells with intact TET1/TET2 enzymes (WT) and MEF cells with TET1/TET2 knocked out (DKO). Our results identify sets of differentially expressed genes which are correlated with TET1/TET2 induced methylation changes of the corresponding genes. Whole transcriptome analysis of M. musculus MEF cells. Two conditions were sequenced and analyzed, the first is wild type (WT), the second corresponds to knock-out of TET1 and TET2 enzymes.

2015-12-07 | E-GEOD-58609 | biostudies-arrayexpress

Combined deficiency of Tet1 and Tet2 is compatible with development but leads to epigenetic instability

2013-02-01 | GSE42396 | GEO

Functional genomic analysis of WT, Tet1-/-, Tet2-/-, Tet1-/-:Tet2-/- (DKO) murine embryonic stem cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-06-26 | GSE122814 | 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

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