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

Zscan10 is dispensable for maintenance of pluripotency in mouse embryonic stem cells

ABSTRACT: Zinc finger and SCAN domain-containing 10 (Zscan10, also known as Zfp206) encodes a transcription factor that has been reported to be involved in the maintenance of pluripotency in mouse embryonic stem (ES) cells. Here we generated inducible knockout ES cells for Zscan10 using the Cre-loxP system and analyzed its function. We succeeded in establishing Zscan10-null ES cells and confirmed their pluripotency by the generation of chimeric embryos. Our results clearly indicate that Zscan10 is dispensable for the ability of self-renewal and differentiation in ES cells. An inducible knockout ES cell line of Zscan10 with the Cre-loxP system was generated and gene expression was measured without Zscan10 deletion or constitutive knocked out cells. Each sample was prepared in triplicate.

ORGANISM(S): Mus musculus

SUBMITTER: Hitoshi Niwa

PROVIDER: E-GEOD-76143 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Zscan10 is dispensable for maintenance of pluripotency in mouse embryonic stem cells.

Yamane Mariko M Fujii Setsuko S Ohtsuka Satoshi S Niwa Hitoshi H

Biochemical and biophysical research communications 20151122 4

Zinc finger and SCAN domain-containing 10 (Zscan10, also known as Zfp206) encodes a transcription factor that has been reported to be involved in the maintenance of pluripotency in mouse embryonic stem (ES) cells. Here we generated inducible knockout ES cells for Zscan10 using the Cre-loxP system and analyzed its function. We succeeded in establishing Zscan10-null ES cells and confirmed their pluripotency by the generation of chimeric embryos. Our results clearly indicate that Zscan10 is dispens ...[more]

PMID: 26592664

Similar Datasets

The C-terminal region of Xpc is dispensable for the transcriptional activity of Oct3/4 in mouse embryonic stem cells

Project description:The transcription factor Oct3/4 is essential to maintain pluripotency in mouse embryonic stem (ES) cells. It was reported that the Xpc DNA repair complex is involved in this process. Here we examined the role of Xpc on the transcriptional activation of the target genes by Oct3/4 using the inducible knockout strategy. We found that the removal of the C-terminal region of Xpc, including the interaction sites with Rad23 and Cetn2, showed faint impact on the gene expression profile of ES cells and the functional Xpc-ΔC ES cell lines retained proper gene expression profile as well as pluripotency to contribute chimeric embryos. These data indicated that the C-terminal region of Xpc is dispensable for the transcriptional activity of Oct3/4 in mouse ES cells. An inducible knockout ES cell line of Xpc with the Cre-loxP system was generated and gene expression was measured without Xpc deletion, after 4 days of Xpc deletion or constitutive knocked out cells. Each sample was prepared in triplicate.

2015-06-09 | E-GEOD-69640 | biostudies-arrayexpress

Zscan10 is dispensable for maintenance of pluripotency in mouse embryonic stem cells

Project description:Zinc finger and SCAN domain-containing 10 (Zscan10, also known as Zfp206) encodes a transcription factor that has been reported to be involved in the maintenance of pluripotency in mouse embryonic stem (ES) cells. Here we generated inducible knockout ES cells for Zscan10 using the Cre-loxP system and analyzed its function. We succeeded in establishing Zscan10-null ES cells and confirmed their pluripotency by the generation of chimeric embryos. Our results clearly indicate that Zscan10 is dispensable for the ability of self-renewal and differentiation in ES cells.

2015-12-20 | GSE76143 | GEO

Gene expression profile after Dax1 deletion in ES cells

Project description:To investigate the function of Dax1 in mouse ES cells, whole genome microarray expression profiling was employed to identify genes that are potentially affected by the deletion of Dax1. An inducible knockout ES cell line of Dax1 with the Cre-loxP system was generated and gene expression was measured (i) without Dax1 deletion, (ii) after 4 days of Dax1 deletion, or (iii) after several passags of Dax1 deletion. Each sample was prepared in triplicate.

2015-05-13 | E-GEOD-61152 | biostudies-arrayexpress

Multiphasic and dynamic changes in alternative splicing during induction of pluripotency are coordinated by numerous RNA binding proteins [ESRP DKO]

Project description:Alternative splicing (AS) plays a critical role in cell fate transitions, development and disease. Recent studies have shown that AS also influences pluripotency and somatic cell reprogramming. We profiled transcriptome-wide AS changes that occur during reprogramming of fibroblasts to pluripotency. This analysis revealed distinct phases of AS during reprogramming, including a splicing program that is unique to transgene-independent iPS cells. Changes in the expression of alternative splicing factors Zcchc24, Esrp1, Mbnl1/2 and Rbm47 were demonstrated to be key contributors to phase-specific AS. RNA binding motif enrichment analysis near alternatively spliced exons provided further insight into the combinatorial regulation of AS during reprogramming by different RNA binding proteins. Ectopic expression of Esrp1 enhanced reprogramming, in part by modulating the AS of the epithelial specific transcription factor Grhl1.These data represent a comprehensive temporal analysis of the dynamic regulation of AS during the acquisition of pluripotency. ES cells from 3 independent E3.5 blastocysts from either Control (Esrp1 WT/WT; Esrp2 -/-) or Esrp DKO (Esrp1 floxed/floxed; Esrp2 -/-) were transfected with pLVX-EGFP-Cre, puro selected and RNA was isolated 6 days later.

2016-03-15 | E-GEOD-76222 | biostudies-arrayexpress

RNA-Seq analysis of mouse small intestine enteroendocrine cells

Project description:We generated knock-in mice expressing GFP under the control of the endogenous GIP (Glucose-dependent Insulinotropic Polypeptide) promoter that enable the isolation of a purified population of small intestine K cells. Using RNA-Seq, we comprehensively characterized the transcriptomes of GIP-GFP cells as well as the entire enteroendocrine lineage derived from Neurogenin3 (Ngn3)-expressing progenitors. We interrogated the whole transcriptome of FACS-isolated small intestine GIPGFP cells using high-throughput mRNA sequencing. We also obtained the global gene expression patterns of the entire enteroendocrine cell lineage as well as the non-enteroendocrine cell population, comprising enterocytes, goblet cells and Paneth cells. To achieve this, small intestine epithelial cells from male mice resulting from the breeding of Neurogenin3 (Ngn3)-Cre mice with ROSA26-LoxP-STOP-LoxP-tomato indicator mice were isolated based on Tomato fluorescence and negative staining for CD45. Due to the small cell numbers, we constructed each of the three RNA-Seq libraries (GIPGFP, Ngn3TOMATO, and Ngn3-) using a pool of equal amounts of individual RNA samples without RNA amplification.

2015-01-01 | E-GEOD-61250 | biostudies-arrayexpress

In vivo analysis of astrocyte ribosome-associated mRNA after traumatic spinal cord injury

Project description:Analysis of gene expression by astrocytes or non-astrocyte cells in spinal cord injury (SCI) lesions may lead to the identification of molecules that impact on axon regrowth. We conducted genome-wide RNA sequencing of (i) immunoprecipitated astrocyte-specific ribosome-associated RNA (ramRNA) from WT or STAT3-CKO astrocytes, and (ii) the non-precipitated (flow-through) RNA deriving from non-astrocyte cells in the same tissue samples 14 days following SCI. DOI: 10.1038/nature17623 Young adult female mGFAP-Cre-RiboTag or mGFAP-Cre-RiboTag-STAT3-LoxP mice underwent severe crush SCI at thoracic level 10. 14 days following SCI, the central 3mm of the SCI lesion was extracted, homogenized and (i) astrocyte-specific ribosome-associated RNA (ramRNA) precipitated via a hemagglutinin (HA) tag targeted to either WT (n=4) or STAT3-CKO (n=3) astrocytes, and (ii) the non-precipitated (flow-through) RNA deriving from non-astrocyte cells in the same tissue samples. Sex and age-matched mGFAP-Cre-RiboTag mice served as uninjured controls (n=4).

2016-03-30 | E-GEOD-76097 | biostudies-arrayexpress

Suppression of ischemia in arterial occlusive disease by JNK-promoted native collateral artery development

Project description:Arterial occlusive diseases are major causes of morbidity and mortality. Blood flow to the affected tissue must be restored quickly if viability and function are to be preserved. Collaterals are artery-to-artery or arteriole-to-arteriole interconnections that can bypass an occlusion by providing an alternative route for blood flow to the affected tissue. The increased flow and sheer stress initiate processes that result in the remodeling (arteriogenesis) of these vessels into efficient conductance arteries. Here we report that the mixed-lineage kinase (MLK) pathway activates cJun NH2-terminal kinase (JNK) in endothelial cells. Disruption of Mlk2/3 or Jnk1/2 genes caused severe blockade of blood flow and failure to recover in the femoral artery ligation model of hindlimb ischemia because of abnormal collateral arteries. We show that the MLK-JNK pathway is essential for patterning and maturation of collateral arteries during development, but this pathway is not required for angiogenesis or arteriogenesis in adults. JNK in endothelial cells promotes Delta-like 4-induced Notch signaling and suppresses excessive sprouting angiogenesis during development. This function of the MLK-JNK pathway contributes to normal formation of native collateral arteries. The MLK-JNK pathway is therefore a key regulatory mechanism for vascular development. These data highlight the crucial importance of the collateral circulation in the response to arterial occlusive diseases. RNA-seq analysis of mouse lung endothelial cells (MLEC) of the following genotypes Cdh5-Cre+ Jnk1+/+ Jnk2+/+ Jnk3-/-(ECtrl), Cdh5-Cre- Jnk1LoxP/LoxP Jnk2LoxP/LoxP Jnk3-/- (EfCtrl), and Cdh5-Cre+ Jnk1LoxP/LoxP Jnk2LoxP/LoxP Jnk3-/- (E3KO). Three separate samples from mouse lung endothelial cells of each genotype were analyzed.

2016-08-09 | E-GEOD-71159 | biostudies-arrayexpress

The C-terminal region of Xpc is dispensable for the transcriptional activity of Oct3/4 in mouse embryonic stem cells

2015-06-09 | GSE69640 | GEO

Deletion of KDM2B DNA-binding domain affects RING1B and SUZ12 occupancy

Project description:The histone lysine demethylase protein, KDM2B, associates with the PCGF1/PRC1 complex and binds to non-methylated DNA through its ZF-CxxC domain, providing a possible molecular link between CpG island elements and polycomb nucleation (Farcas et al., 2012, Wu et al., 2013). Here, a novel genetic system was designed in which PCGF1/PRC1 targeting could be disrupted in vivo through the ablation of KDM2B-mediated DNA binding. To ablate PCGF1/PRC1 targeting, an exon that encodes most of the KDM2B ZF-CxxC domain and is shared by both the long and short form of the protein was flanked by loxP sites (Kdm2bfl/fl). Homozygous mouse ES cell lines were derived that also stably express a tamoxifen inducible form of CRE-recombinase. CRE induced deletion of the ZF-CxxC domain by the addition of tamoxifen yields KDM2B long and short form proteins that are incapable of binding to CpG island DNA but still remain associated with the PCGF1/PRC1 variant complex. We then assessed genome-wide occupancy of the PRC1 component RING1B and the PRC2 component SUZ12 to examine the impact of losing KDM2B-dependent targeting of polycomb. KDM2Bfl/fl ES cells were treated with 800M-BM-5M tamoxifen for 72hours and compared to untreated control cells by ChIP-seq for KDM2B, RING1B and SUZ12, and RNA-seq.

2014-05-27 | E-GEOD-52619 | biostudies-arrayexpress

Rex1/Zfp42 is dispensable for pluripotency in mouse ES cells

Project description:We showed the function of Rex1 in mouse ES cells as well as in embryos using the conventional gene targeting strategy. Our results clearly indicated that Rex1 function is dispensable for both the maintenance of pluripotency in ES cells and the development of embryos. However, Rex1-/- ES cells showed the defect to induce a subset of the marker genes of visceral endoderm, when differentiated as embryoid body, as found in EC cells. Conclusion: Rex1 should be regarded just as a marker of pluripotency without functional significance like the activity of alkaline phosphatase. Keywords: genetic modification design,reference design,replicate design

2008-09-13 | GSE12753 | 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