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Abscission couples cell division to embryonic stem cell fate

ABSTRACT: Abscission couples cell division to embryonic stem cell fate

PROVIDER: PRJNA594885 | ENA |

REPOSITORIES: ENA

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Abscission Couples Cell Division to Embryonic Stem Cell Fate.

Project description: Not available

| S-EPMC7594744 | biostudies-literature

The Cdk-activating kinase (CAK) couples cell growth to cell division

Project description:We report that inactivation of the fission yeast Cdk7 kinase affects gene expression through both its RNA Polymerase II CTD kinase activity and its Cdc2-activating kinase activity. The ribosome biogenesis cluster is specifically downregulated when Cdc2 T167 phosphorylation is abolished, which results is slow growth. We propose that Cdc2 activation by CAK defines the rate change point observed in mid G2 and that CAK therefore couples cell growth to cell division. Total RNA was isolated from two biological replicates for all conditions, and each biological replicate was hybridized in duplicate on Agilent arrays (dye-swap).

2012-02-19 | E-GEOD-27425 | biostudies-arrayexpress

Abscission couples cell division to embryonic stem cell fate

Project description:This study was designed to investigate how the cell cycle phase impacts the kinetics of exit from pluripotency of mouse embryonic stem cells (mESC). mESC maintained in naïve medium conditions (2i) then sorted based on cell cycle phase before replating in self-renewing or differentiating media for 6hours, followed by single-cell RNA sequencing. Clustering of cells based on their expression of naive pluripotency genes indicate that cells that exit early in the cell cycle downregulate pluripotency genes faster than the bulk population. This study provides evidence that cell cycle phase is important in determining the timing of exit from pluripotency.

2020-09-13 | GSE141811 | GEO

An organelle-tethering mechanism couples flagellation to cell division in bacteria

Project description:An organelle-tethering mechanism couples flagellation to cell division in bacteria

| PRJNA644624 | ENA

An organelle-tethering mechanism couples flagellation to cell division in bacteria

Project description:In both free-living and pathogenic bacteria, problems in the synthesis and assembly of early flagellar components invariably lead to cell division defects. However, the mechanism that fine-tunes the cell division cycle with the flagellar biogenesis is poorly understood. Herein, we report the role of the conserved regulator MadA in coupling flagellar biogenesis to cell division in Caulobacter crescentus. We demonstrate that MadA is required to induce the flagellar specific type III export component FlhA to release and activate FliX, which in-turn is required to license the conserved σ54-activator, FlbD. In the absence of MadA, FliX is tethered to FlhA, inhibiting FlbD activation and crippling completion of flagellar biogenesis and cell division. Furthermore, we demonstrate that MadA exploits a divisome-stoichiometric to control cell division. We propose that MadA has a sentinel-type function that warrants progression of the flagellar biogenesis, and the cell division cycle, once early flagellar structures are properly assembled.

2021-02-18 | GSE153968 | GEO

Metabolic determination of cell fate through selective inheritance of mitochondria

Project description:Metabolic characteristics of adult stem cells are distinct from their differentiated progeny, and cellular metabolism is emerging as a potential driver of cell fate conversions. However, how metabolism influences fate determination remains unclear. Here, we identified inherited metabolism imposed by functionally distinct mitochondrial age-classes as a fate determinant in asymmetric division of epithelial stem-like cells. While chronologically old mitochondria support oxidative respiration, new organelles are immature and metabolically less active. Upon cell division, selectively segregated mitochondrial age-classes elicit a metabolic bias in progeny cells, with old mitochondria imposing oxidative energy metabolism inducing differentiation. High pentose phosphate pathway flux, promoting redox maintenance, is favoured in cells receiving newly synthesised mitochondria, and is required to maintain stemness during early fate determination after division. Our results demonstrate that fate decisions are susceptible to intrinsic metabolic bias imposed by selectively inherited mitochondria.

2021-12-20 | PXD010667 | Pride

Asymmetric division of contractile domains couples cell positioning and fate specification.

Project description: Not available

| S-EPMC4998956 | biostudies-literature

Yap1-Scribble polarization is required for hematopoietic stem cell division and fate

Project description:Yap1-Scribble polarization is required for hematopoietic stem cell division and fate

| PRJNA635915 | ENA

Cytokine receptor-Eb1 interaction couples cell polarity and fate during asymmetric cell division.

Project description: Not available

| S-EPMC5886756 | biostudies-literature

Yap1-Scribble polarization is required for hematopoietic stem cell division and fate

Project description:Yap1 and its paralogue Taz largely control epithelial tissue growth. We have identified that hematopoietic stem cell (HSC) fitness response to stress depends on Yap1 and Taz. Deletion of Yap1 and Taz induces a loss of HSC quiescence, symmetric self-renewal ability and renders HSC more vulnerable to serial myeloablative 5-fluorouracil treatment. This effect depends on the predominant cytosolic polarization of Yap1 through its PDZ domain-mediated interaction with the scaffold Scribble. Scribble and Yap1 coordinate to control cytoplasmic Cdc42 activity and HSC fate determination in vivo. Deletion of Scribble disrupts Yap1 co-polarization with Cdc42 and decreases Cdc42 activity, resulting in increased selfrenewing HSC with competitive reconstitution advantages. These data suggest that Scribble/Yap1 co-polarization is indispensable for Cdc42- dependent activity on HSC asymmetric division and fate. The combined loss of Scribble, Yap1 and Taz results in transcriptional upregulation of Rac-specific guanine nucleotide exchange factors, Rac activation and HSC fitness restoration. Scribble links Cdc42 and the cytosolic functions of the Hippo signaling cascade in HSC fate determination.

2020-05-30 | GSE151465 | GEO

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