Cell competition regulates the fate decision of neural stem cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA925106 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cell competition is a new notion of old theory Darwinian theory in cell level. It is notorious as its function on cancer promotion, actually, cell competition is a critical checkpoint machinery in development, its proper operation roles out suboptimal cells and makes sure the high quality of basic materials make up organism. Although its function has been revealed on other organs, it remains mysterious in brain development. In this paper, we get a compromised cell competitional model by knocking out endothelial Brd4, the lack of Brd4 in endothelial cell induces less neural stem cells deaths and compromised cell competition, endothelial Brd4 regulates cell competition is Testican2 dependent, Testican2 can deposit Sparc. We find a noncanonical role of the canonical negative cell competitional regulator Sparc in the fate decision of neural stem cells, neural stem cells highly expressing Sparc steps forward differentiation. We also find a compromised cell competition in AD patients, by cloning a point mutant of Brd4 found in a group of AD, we reveals that the mutant lose the potential of cell competition promotion. We put forward a new strategy for the treatment of aging related diseases by enhancing cell competitional state.
2023-01-25 | GSE223131 | GEO
Project description:Bcl6 regulates CD8+ T cell fate decision in cancer [RNA-Seq]
| PRJNA754303 | ENA
Project description:Bcl6 regulates CD8+ T cell fate decision in cancer [ChIP-Seq]
| PRJNA754302 | ENA
Project description:Telomere Shortening Impairs PGC Fate Decision
| PRJNA660792 | ENA
Project description:Neural stem cells (NSCs) generate neurons and glial cells throughout embryonic and postnatal brain development. The role of s-acylation, a reversible post-translational lipid modification of proteins, in regulating fate and activity of NSCs remains largely unknown. We here used an unbiased screening approach to identify proteins that are s-acylated in mouse NSCs.
2019-11-27 | PXD014355 | Pride
Project description:Transcription factor KLF2 regulates cell fate decision of stem cells in infantile hemangioma
| PRJNA998877 | ENA
Project description:Hypoxia augments human embryonic stem cell self-renewal via hypoxia-inducible factor 2M-NM-1 (HIF2M-NM-1) activated OCT4 (POU5F1) transcription. Hypoxia also increases the efficiency of reprogramming differentiated cells to a pluripotent-like state. Combined, these findings suggest that low oxygen (O2) tension would impair the purposeful differentiation of pluripotent stem cells. Here, we show that low O2 tension and HIF activity instead promotes appropriate hESC differentiation. Through gain and loss of function studies, we implicate O2 tension as a modifier of a key cell fate decision, namely whether neural progenitors differentiate towards neurons or glia. Furthermore, our data show that even transient changes in O2 concentration can affect cell fate through HIF by regulating the activity of MYC, a regulator of LIN28/let-7 that is critical for fate decisions in the neural lineage. We also identify key small molecules that can take advantage of this pathway to quickly and efficiently promote the development of mature cell types. We used microarrays to detail the global gene expression of human neural progenitor cells (NPC) cultured in physiological (2%) oxygen tension. By comparing NPCs with activated Hypoxia inducible factor (HIF) activity (DFX treatment) and NPCs with diminished HIF activity (HIF1M-NM-2 knockdown), we identified genes that are important for NPC fate decision under physiological oxygen concentration. We also used microarrays to obtain a global gene expression profiling during embryoid bodies formation using ES cells with diminished HIF activity. In HIF activation experiments, two ES lines and one iPS line-derived NPC were used, with or without DFX treatment for 5 days. In HIF1M-NM-2 knockdown experiments, NPCs were derived from either shHIF1M-NM-2 or control ES lines. In embryoid body formation experiments, day0 (ES stage) and day6 EBs were generated from either shHIF1M-NM-2 or control ES lines in 2% oxygen.
2014-09-30 | E-GEOD-61842 | biostudies-arrayexpress
Project description:Telomere Shortening Impairs PGC Fate Decision [ATAC-seq]
| PRJNA660789 | ENA
Project description:Telomere Shortening Impairs PGC Fate Decision [RNA-seq]
| PRJNA660794 | ENA
Project description:Neural crest cells are embryonic progenitors that generate numerous cell types in vertebrates. With single cell analysis, we show that mouse trunk neural crest cells become biased toward neuronal lineages when they delaminate from the neural tube, whereas cranial neural crest cells acquire ectomesenchyme potential dependent on activation of the transcription factor Twist1. The choices that neural crest cells make to become sensory, glial, autonomic, or mesenchymal cells can be formalized as a series of sequential binary decisions. Each branch of the decision tree involves initial co-activation of bipotential properties followed by gradual shifts towards commitment. Competing fate programs are co-activated before cells acquire fate-specific phenotypic traits. Determination of a specific fate is achieved by increased synchronization of relevant programs and concurrent repression of competing fate programs.
2019-04-02 | GSE129114 | GEO