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

PROVIDER: PRJNA885142 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21743282.fastq.gz	Fastqsanger.gz
	SRR21743283.fastq.gz	Fastqsanger.gz
	SRR21743284.fastq.gz	Fastqsanger.gz
	SRR21743285.fastq.gz	Fastqsanger.gz
	SRR21743286.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 11

Similar Datasets

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

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

| PRJNA789532 | ENA

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

Project description: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).

2022-10-01 | GSE214402 | GEO

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

Project description:TET (Ten-Eleven Translocation) dioxygenases effect DNA demethylation through successive oxidation of the methyl group of 5-methylcytosine (5mC) in DNA. In humans and in mouse models, TET loss-of-function has been linked to DNA damage, genome instability and oncogenesis. Here we show that acute deletion of all three Tet genes, after brief exposure of triple-floxed, Cre-ERT2-expressing mouse embryonic stem cells (mESC) to 4-hydroxytamoxifen, results in chromosome mis-segregation and aneuploidy; moreover, embryos lacking all three TET proteins showed striking variation in blastomere numbers and nuclear morphology at the 8-cell stage. Transcriptional profiling revealed that mRNA encoding a KH-domain protein, Khdc3 (Filia), was downregulated in triple TET-deficient mESC, concomitantly with increased methylation of CpG dinucleotides in the vicinity of the Khdc3 gene. Restoring KHDC3 levels in triple Tet-deficient mESC prevented aneuploidy. Thus, TET proteins regulate Khdc3 gene expression, and TET deficiency results in mitotic infidelity and genome instability in mESC at least partly through decreased expression of KHDC3.

| S-EPMC9584922 | biostudies-literature

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

Khdc3 Regulates Metabolism Across Generations in a DNA-Independent Manner

Project description:Genetic variants can alter the profile of heritable molecules such as small RNAs in sperm and oocytes, and in this manner ancestral genetic variants can have a significant effect on offspring phenotypes even if they are not themselves inherited. Here we show that wild type female mice descended from ancestors with a mutation in the mammalian germ cell gene Khdc3 have hepatic metabolic defects that persist over multiple generations. We find that genetically wild type females descended from Khdc3 mutants have transcriptional dysregulation of critical hepatic metabolic genes, which persist over multiple generations and pass through both female and male lineages. This was associated with dysregulation of hepatically-metabolized molecules in the blood of these wild type mice with mutational ancestry. The oocytes of Khdc3-null females, as well as their wild type descendants, had dysregulation of multiple small RNAs, suggesting that these epigenetic changes in the gametes transmit the phenotype between generations. Our results demonstrate that ancestral mutation in Khdc3 can produce transgenerational inherited phenotypes, potentially indefinitely.

2025-01-31 | GSE288429 | GEO

Khdc3 Regulates Metabolism Across Generations in a DNA-Independent Manner

2025-01-30 | GSE281631 | GEO

Khdc3 Regulates Metabolism Across Generations in a DNA-Independent Manner [liver]

2025-01-30 | GSE282184 | GEO

Khdc3 Regulates Metabolism Across Generations in a DNA-Independent Manner [II]

2025-01-31 | GSE288414 | GEO

Khdc3 Regulates Metabolism Across Generations in a DNA-Independent Manner [small RNA-seq]

2025-01-30 | GSE287350 | GEO

Khdc3 Regulates Metabolism Across Generations in a DNA-Independent Manner [WTMM, WTPP, HFP liver RNA-seq]

2025-01-30 | GSE283285 | GEO