Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA155007 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:ECAT15-2/Dppa2 transgenic rescue into ECAT15-2/Dppa2 deficient ESCs
| PRJNA155003 | ENA
Project description:This SuperSeries is composed of the following subset Series: GSE31581: ECAT15-2/Dppa2 deficient ESCs GSE31582: ECAT15-2/Dppa2 transgenic rescue into ECAT15-2/Dppa2 deficient ESCs GSE31583: Lung of ECAT15-2/Dppa2 deficient embryo at E18.5 Refer to individual Series
2011-10-16 | E-GEOD-31584 | biostudies-arrayexpress
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Lipid metabolism is recognized as a key process for stem cell maintenance and differentiation but genetic factors that instruct stem cell function by influencing lipid metabolism remain to be delineated. Here we identify Tnfaip2 as an inhibitor of reprogramming of mouse fibroblasts into induced pluripotent stem cells. Tnfaip2 knockout embryonic stem cells (ESCs) exhibit differentiation failure and knockdown of the planarian orthologue, Smed-exoc3, abrogates in vivo differentiation of somatic stem cells, tissue homeostasis, and regeneration. Tnfaip2 deficient ESCs fail to induce synthesis of cellular triacylglycerol (TAG) and lipid droplets (LD) coinciding with reduced expression of Vimentin (Vim) – a known inducer of LD formation. Knockdown of Vim and Tnfaip2 act epistatically in enhancing cellular reprogramming of mouse fibroblasts. Similarly, planarians devoid of Smed-exoc3 displayed acute loss of TAGs. Supplementation of palmitic acid (PA) and palmitoyl-L-carnitine (a mitochondrial carrier of PA) restores the differentiation capacity of Tnfaip2 deficient ESCs as well as stem cell differentiation and organ maintenance in Smed-exoc3-depleted planarians. Together, these results identify a novel pathway, which is essential for stem cell differentiation and organ maintenance by instructing lipid metabolism.
2020-11-16 | GSE134301 | GEO
Project description:Lipid metabolism is recognized as a key process for stem cell maintenance and differentiation but genetic factors that instruct stem cell function by influencing lipid metabolism remain to be delineated. Here we identify Tnfaip2 as an inhibitor of reprogramming of mouse fibroblasts into induced pluripotent stem cells. Tnfaip2 knockout embryonic stem cells (ESCs) exhibit differentiation failure and knockdown of the planarian orthologue, Smed-exoc3, abrogates in vivo differentiation of somatic stem cells, tissue homeostasis, and regeneration. Tnfaip2 deficient ESCs fail to induce synthesis of cellular triacylglycerol (TAG) and lipid droplets (LD) coinciding with reduced expression of Vimentin (Vim) – a known inducer of LD formation. Knockdown of Vim and Tnfaip2 act epistatically in enhancing cellular reprogramming of mouse fibroblasts. Similarly, planarians devoid of Smed-exoc3 displayed acute loss of TAGs. Supplementation of palmitic acid (PA) and palmitoyl-L-carnitine (a mitochondrial carrier of PA) restores the differentiation capacity of Tnfaip2 deficient ESCs as well as stem cell differentiation and organ maintenance in Smed-exoc3-depleted planarians. Together, these results identify a novel pathway, which is essential for stem cell differentiation and organ maintenance by instructing lipid metabolism.
2020-11-16 | GSE148758 | GEO
Project description:Lung of ECAT15-2/Dppa2 deficient embryo at E18.5
| PRJNA155005 | ENA
Project description: Not available
| S-EPMC11335981 | biostudies-literature
Project description:The molecular mechanism controlling the zygotic genome activation (ZGA) in mammals remains poorly understood. The 2C-like cells spontaneously emerging from cultures of mouse embryonic stem cells (ESCs) share some key transcriptional and epigenetic programs with 2-cell stage embryos. By studying the transition of ESCs into 2C-like cells, we identified Dppa2/4 as important regulators controlling zygotic transcriptional program through directly upregulating the expression of Dux. In addition, we found that DPPA2 protein is sumoylated and its activity is negatively regulated by Sumo E3 ligase PIAS4. PIAS4 is downregulated during zygotic genome activation process and during transitioning of ESCs into 2C-like cells. Depleting Pias4 or overexpressing Dppa2/4 is sufficient to upregulateactivate 2C-like transcriptional program, while depleting Dppa2/4 or forced expression of PIAS4 or Sumo2-Dppa2 inhibits 2C-like transcriptional program. Furthermore, ectopic expression of Pias4 or Sumo2-Dppa2 impairs early mouse embryo development. In summary, our study identifies key molecular rivals consisting of transcription factors and a Sumo2 E3 ligase that regulate the transition of ESCs into 2C-like cells and zygotic transcriptional program upstream of Dux.
2019-03-06 | PXD012925 | Pride
Project description:Dppa2 (Developmental pluripotency associated 2), specifically expressed in embryonic stem cells (ESCs) and reactivated in certain cancers, plays important roles in regulating the transition between pluripotency and differentiation. However, its involvement in the DNA damage response (DDR) of mouse ESCs (mESCs) has remained unclear. Here, we identify a surprising pro-apoptotic function for Dppa2 as a novel p53-interacting partner in mESCs. Dppa2 physically interacts with p53 and is transcriptionally repressed by p53 upon DNA damage. By comparing the effects of Dppa2 in p53+/+ and p53-/- mESCs, we find that Dppa2 promotes DNA damage-induced apoptosis (DIA) of mESCs in a p53-dependent manner. RNA-seq and chromatin immunoprecipitation followed by sequencing (ChIP-seq) reveal that Dppa2 and p53 co-repress genes involved in cell cycle regulation and self-renewal, which are highly expressed in ESCs. Mechanistically, Dppa2 recruits p53 to the enhancers of these co-repressed genes. Consequently, Dppa2 depletion significantly compromises p53’s binding intensity and alleviates transcriptional repression. Collectively, our findings uncover a novel mechanism of p53-mediated apoptosis achieved through cooperation with its ESC-specific partner, Dppa2, thereby highlighting a previously unappreciated tumor suppressor identity of Dppa2.
2025-07-12 | GSE301903 | GEO
Project description: Not available
| S-EPMC4490682 | biostudies-literature