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Spatio-temporal structure of cell fate decisions in murine neural crest

ABSTRACT: Spatio-temporal structure of cell fate decisions in murine neural crest

PROVIDER: PRJNA530171 | ENA |

REPOSITORIES: ENA

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Spatio-temporal structure of cell fate decisions in murine neural crest

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

The dynamics of Atm signalling dictate cellular fate decisions after DNA damage

Project description:DNA damage activates diverse cellular responses â€“ either protective or deleterious â€“that ultimately promote or inhibit proliferation. How the distinct responses conferring crucial cell fate decisions are chosen is unclear. Using a systems approach, we demonstrate that the dynamic features of Atm dependent DNA double-strand break (DSB) signalling response dictate cellular outcome. Combining temporal phosphoproteome and nascent transcriptome analyses after low or high DNA-damage-load, we discovered that some responses, such as Tp53 activation, have an activation threshold and others arise independently of DNA-damage-load. Using DSB repair deficient cells, we show that persistent DSBs alter the kinetics â€“ but not the amplitude â€“ of Atm signalling. Thus, we demonstrate that pathway choices are dictated by the signalling dynamics and hence cell fate decisions are responsive to DNA-damage-load and repair capacity of the cells.

2023-01-18 | PXD013620 | Pride

O-GlcNAc Homeostasis Controls Cell Fate Decisions During Hematopoiesis

Project description:O-GlcNAc Homeostasis Controls Cell Fate Decisions During Hematopoiesis

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Local lung hypoxia determines epithelial fate decisions during alveolar regeneration

Project description:Local lung hypoxia determines epithelial fate decisions during alveolar regeneration

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Suppressive and stimulatory host processes during virus infection fate decisions

Project description:Suppressive and stimulatory host processes during virus infection fate decisions

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Hippo pathway and Bonus control developmental cell fate decisions in the Drosophila eye

Project description:The canonical function of the Hippo signaling pathway is the regulation of organ growth. How this pathway controls cell fate determination is less well understood. Here, we identify a function of the Hippo pathway in cell fate decisions in the developing Drosophila eye, exerted through the interaction of Yorkie (Yki) with the transcriptional regulator Bonus (Bon), an ortholog of mammalian Transcriptional Intermediary Factor 1/tripartite motif (TIF1/TRIM) family proteins. Instead of controlling tissue growth, Yki and Bon promote epidermal and antennal fates at the expense of the eye fate. Proteomic, transcriptomic, and genetic analyses reveal that Yki and Bon control these cell fate decisions by recruiting transcriptional and post-transcriptional co-regulators, and by repressing Notch target genes and activating epidermal differentiation genes. Our work expands the range of functions and regulatory mechanisms under Hippo pathway control.

2023-01-17 | GSE181299 | GEO

In vivo CRISPR screening reveals nutrient signaling processes underpinning CD8+ T cell fate decisions [microarray_dataset1]

Project description:The role of nutrient signaling processes in the fate decision of CD8 is incompletely understood. By performing in vivo pooled CRISPR-Cas9 screening, we uncovered nutrient signaling processes underpinning the dynamics and heterogeneity of CD8 T cell fate decisions.

2021-02-25 | GSE148681 | GEO

In vivo CRISPR screening reveals nutrient signaling processes underpinning CD8+ T cell fate decisions [Pofut1_microarray]

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In vivo CRISPR screening reveals nutrient signaling processes underpinning CD8+ T cell fate decisions [NICD_microarray]

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Notch-HES1 signaling axis controls hemato-endothelial fate decisions of human embyronic and induced pluripotent cells

Project description:Notch signaling regulates several cellular processes including cell fate decisions and proliferation in both invertebrates and mice. However, comparatively less is known about the role of Notch during early human development. Here, we examined the function of Notch signaling during hematopoietic lineage specification from human pluripotent stem cells (hPSCs) of both embryonic and adult fibroblast origin. Using immobilized Notch ligands and siRNA to Notch receptors we have demonstrated that Notch1, but not Notch2 activation, induced HES1 expression and generation of committed hematopoietic progenitors. Using gain and loss of function approaches, this was shown to be attributed to Notch signaling regulation through HES1, that dictated cell fate decisions from bipotent precursors either to the endothelial or hematopoietic lineages at the clonal level. Our study reveals a previously unappreciated role for the Notch pathway during early human hematopoiesis, whereby Notch signaling via HES1 represents a toggle switch of hematopoietic vs. endothelial fate specification. Human pluripotent stem cells (hPSCs) have differentiation potential into three embryonic germ layers including blood. Notch signaling is one of important signaling pathways involved in blood differentiation of hPSCs. Thus, in order to examine the effect of Notch signaling pathways during hematopoietic differentiation of hPSCs, embryoid bodies (EBs) were formed and cultured for 10 days in the combination of cytokines and growth factors (Chadwick, Blood, 2003; 300 ng/ml of SCF, 300 ng/ml of Flt-3L, 10 ng/ml of IL-3, 10 ng/ml of IL-6, and 50 ng/ml of G-CSF) to induce differentiation into blood. Additionally, CD31+CD45- bipotent hemogenic precursors were isolated from day10 hematopoietic EBs (Wang et al., Immunity, 2004)

2013-06-01 | E-GEOD-47466 | biostudies-arrayexpress

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