Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Acute deletion of TET enzymes results in aneuploidy in mouse embryonic stem cells through decreased expression of Khdc3 (Whole Genome Sequencing [Low Coverage])

ABSTRACT: Low coverage whole genome sequencing (lc-WGS) from inducible Tet TKO (Tet iTKO) and control (Ctrl) mouse ESCs (mESC), as well as for germline Dnmt TKO mESCs. mESCs were sorted to isolate the Live/Dead dye and Thy1.2 negative CD326+GFP+ population representing the mESCs populations responsive to the tamoxifen treatment. The cells were resuspended in FACS buffer and filtered with a 70 µM filter before sorting. These bulk-population samples were analyzed by using low coverage Whole Genome Sequencing (lc-WGS).

ORGANISM(S): Mus musculus

PROVIDER: GSE214402 | GEO | 2022/10/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Acute deletion of TET enzymes results in aneuploidy in mouse embryonic stem cells through decreased expression of Khdc3

Project description:Gene expression with RNA-seq for inducible Tet TKO (Tet iTKO) mESCs compared with control mouse ESCs (mESC) after 6.5 days in vitro culture after tamoxifen treatment

2022-10-28 | GSE191045 | GEO

Evaluation of copy number variation detection between high-resolution array CGH and low-coverage short-insert and mate-pair whole-genome sequencing

Project description:In principle, whole-genome sequencing (WGS) of the human genome even at low coverage offers higher resolution for genomic copy number variation (CNV) detection compared to array-based technologies, which is currently the first-tier approach in clinical cytogenetics. There are, however, obstacles in replacing array-based CNV detection with that of low-coverage WGS such as cost, turnaround time, and lack of systematic performance comparisons. With technological advances in WGS in terms of library preparation, instrument platforms, and data analysis algorithms, obstacles imposed by cost and turnaround time are fading. However, a systematic performance comparison between array and low-coverage WGS-based CNV detection has yet to be performed. Here, we compared the CNV detection capabilities between WGS (short-insert, 3kb-, and 5kb-mate-pair libraries) at 1X, 3X, and 5X coverages and standardly used high-resolution arrays in the genome of 1000-Genomes-Project CEU genome NA12878. CNV detection was performed using standard analysis methods, and the results were then compared to a list of Gold Standard NA12878 CNVs distilled from the 1000-Genomes Project. Overall, low-coverage WGS is able to detect drastically more (approximately 5 fold more on average) Gold Standard CNVs compared to arrays and is accompanied with fewer CNV calls without secondary validation. Furthermore, we also show that WGS (at ≥1X coverage) is able to detect all seven validated deletions larger than 100 kb in the NA12878 genome whereas only one of such deletions is detected in most arrays. Finally, we show that the much larger 15 Mbp Cri-du-chat deletion can be clearly seen at even 1X coverage from short-insert WGS.

2018-06-26 | GSE105092 | GEO

Affymetrix CytoScan 750K and HD data for developmental delay and/or physical disability phenotypes samples

Project description:Chromosomal copy number variations (CNV) have been associated with various neurological and developmental disorders and chromosomal microarray (CMA) is a method of choice to diagnose Copy Number Gain/Loss syndromes. Recently, next-generation sequencing (NGS)-based low-coverage whole genome sequencing (LC-WGS) has been applied to detect Copy Number Gain/Loss syndromes. This dataset is intended to be used as a “Golden standard data set” for development of LC-WGS analysis method. It consists of patients (n=63) who have a mental delay and/or physical disability phenotype and normal (n=20) phenotype.

2018-09-29 | GSE120624 | GEO

Inducible disruption of Tet genes results in myeloid malignancy, readthrough transcription, and a heterochromatin-to-euchromatin switch [Hi-C]

Project description:The three mammalian TET dioxygenases oxidize the methyl group of 5-methylcytosine (5mC) in DNA, and the oxidised methylcytosines are essential intermediates in all known pathways of DNA demethylation. To define the in vivo consequences of complete TET deficiency, we inducibly deleted all three Tet genes in the mouse genome. Tet1/2/3 inducible TKO (iTKO) mice succumbed to acute myeloid leukaemia by 4-5 weeks. Single-cell RNA sequencing of Tet iTKO bone marrow cells revealed the appearance of new myeloid cell populations characterised by a striking increase in expression of all members of the stefin/cystatin gene cluster on mouse chromosome 16. In patients with acute myeloid leukaemia, high stefin/cystatin gene expression correlates with poor clinical outcomes. Increased expression of the clustered stefin/cystatin genes was associated with a heterochromatin-to-euchromatin compartment switch with readthrough transcription downstream of the clustered stefin/cystatin genes as well as other highly expressed genes but only minor changes in DNA methylation. Our data highlight new roles for TET enzymes that are distinct from their established function in DNA demethylation, and instead involve increased transcriptional readthrough and changes in three-dimensional genome organisation.

2023-04-18 | GSE222719 | GEO

Inducible disruption of Tet genes results in myeloid malignancy, readthrough transcription, and a heterochromatin-to-euchromatin switch [ATAC-seq]

2023-04-18 | GSE222718 | GEO

Inducible disruption of Tet genes results in myeloid malignancy, readthrough transcription, and a heterochromatin-to-euchromatin switch [WGBS]

2023-04-18 | GSE222725 | GEO

Inducible disruption of Tet genes results in myeloid malignancy, readthrough transcription, and a heterochromatin-to-euchromatin switch [scRNA-seq]

2023-04-18 | GSE222722 | GEO

Inducible disruption of Tet genes results in myeloid malignancy, readthrough transcription, and a heterochromatin-to-euchromatin switch [Ribodepleted RNA-seq]

2023-04-18 | GSE222721 | GEO

Inducible disruption of Tet genes results in myeloid malignancy, readthrough transcription, and a heterochromatin-to-euchromatin switch [polyA+ RNA-seq]

2023-04-18 | GSE222720 | GEO

Loss of Tet enzymes compromises proper differentiation of embryonic stem cells

Project description:Tet enzymes (Tet1/2/3) convert 5-methylcytosine (5mC) to 5-hydroxy-methylcytosine (5hmC) and are dynamically expressed in various embryonic and adult cell types. While loss of individual Tet enzymes or combined deficiency of Tet1/2 allows for embryogenesis, the effect of complete loss of Tet activity and 5hmC marks in development is not established. We have generated Tet1/2/3 triple knockout (TKO) mouse embryonic stem cells (ESCs) and examined their developmental potential. Combined deficiency of all three Tets depleted 5hmC and impaired ESC differentiation as seen in poorly differentiated TKO embryoid bodies (EBs) and teratomas. Consistent with impaired differentiation, TKO-ESCs contributed poorly to chimeric embryos and could not support embryonic development. Global gene expression and methylome analyses of TKO-EBs revealed promoter hypermethylation and deregulation of genes implicated in embryonic development and differentiation. These findings suggest a requirement for Tet- and 5hmC-mediated DNA demethylation in proper regulation of gene expression during differentiation of ESCs and development. To quantify global gene expression in differentiating embryoid bodies (EBs) derived from wild type (WT) and Tet triple knockout (TKO), TKO and WT mouse embryonic stem cells (ESCs) were differentiated in vitro to EBs and cultured for 10 days. RNA was extracted using Qiagen RNeasy kit and subjected to microarray analysis. Global gene expression profile of two technical replicas of WT embryoid bodies (2 samples in total) was compared to two technical replicas of two independent TKO embryoid bodies (4 TKO samples in total).

2014-04-14 | E-GEOD-55574 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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