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Genetic reporter for live tracing fluid flow forces during cell fate segregation in mouse blastocyst development [scRNA-seq]

ABSTRACT: We performed single-cell RNA-seq in cultured embryos under shaking and static condition using Klf2-H2Bmcherry mice to screen an effective force reporter.

ORGANISM(S): Mus musculus

PROVIDER: GSE197168 | GEO | 2023/07/31

REPOSITORIES: GEO

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Genetic reporter for live tracing fluid flow forces during cell fate segregation in mouse blastocyst development

Project description:We used a robut low input cell and high throughput in-situ ChIP method to emphasize regulation mechanism among E3.5 klf2, E3.5 klf4 and E12.5 EC klf2.

2023-07-31 | GSE197167 | GEO

Genetic reporter for live tracing fluid flow forces during cell fate segregation in mouse blastocyst development

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Genetic reporter for live tracing fluid flow forces during cell fate segregation in mouse blastocyst development

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Genetic reporter for live tracing fluid flow forces during cell fate segregation in mouse blastocyst development

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Genetic reporter for live tracing fluid flow forces during cell fate segregation in mouse blastocyst development [scRNA-seq]

Project description:Genetic reporter for live tracing fluid flow forces during cell fate segregation in mouse blastocyst development [scRNA-seq]

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Differentiating erythroblasts adapt to turbulent flow by accelerating maturation and activating cholesterol biosynthesis.

Project description:In vitro culture of erythroblasts and production of mature erythrocytes for transfusion purposes requires upscaling in bioreactors with turbulent fluidic environments, resulting in membrane shear stress. For the implementation of erythroid cultures in bioreactors, further understanding of the effects of mechanical stress on terminal erythroblast differentiation are required. To this end, we investigated the effect of orbital shaking-induced shear stress on differentiation of CD49d+CD235low primary human erythroblast (EBL) towards enucleated reticulocytes at the molecular, cellular, and functional level. Orbital shaking at the onset of erythroblast differentiation enhanced cell maturation and increased enucleation percentage compared to static cultures, without loss of cell viability. Transcriptome analysis uncovered 505 genes to be differentially expressed between static and non-static cultures, where genes involved in lipids and cholesterol biosynthesis pathways where upregulated in non-static conditions. In line with this finding, cells differentiated in orbital shakers showed an increased cholesterol concentration and higher osmotic resistance compared to cells differentiated in static condition. HMGCR (3-Hydroxy-3-Methylglutaryl-CoA-Reductase), a rate limiting enzyme of the cholesterol biosynthesis pathway, is significantly increased and showed earlier induction during differentiation in shear stress environments. Inhibition of HMGCR using lovastatin led to severe loss of EBL differentiation in shear environments but not in static conditions. In conclusion, differentiating EBL display a dynamic capability to adapt to shear stress environments, by modulating their transcriptional program and consequently upregulating cholesterol biosynthesis, which is critical for their survival. This work sheds light into specific mechanisms which will assist on the successful upscaling of erythroid differentiation in turbulent bioreactors.

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A dual-fluorescence reporter in the Eomes locus for live imaging and medium-term lineage tracing.

Project description:The T-box transcription factor Eomes (also known as Tbr2) shows short-lived expression in various localized domains of the embryo, including epiblast cells during gastrulation and intermediate progenitor cells in the cerebral cortex. In these tissues Eomes fulfills crucial roles for lineage specification of progenitors. To directly observe Eomes-dependent cell lineages in the living embryo, we generated a novel dual-fluorescence reporter allele that expresses a membrane-bound tdTomato protein for investigation of cell morphology and a nuclear GFP for cell tracing. This allele recapitulates endogenous EOMES protein expression and is suitable for live imaging. We found that the allele can also be used as a short-to-medium-term lineage tracer, as GFP persists in cells longer than EOMES protein and marks Eomes-dependent lineages with a timeframe of days to weeks depending on the proliferation rate. In summary, we present a novel genetic tool for investigation of Eomes-dependent cell types by live imaging and lineage tracing.

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KLF2-induced actin shear fibers control both alignment to flow and JNK signaling in vascular endothelium

Project description:The shear stress-induced transcription factor KrÃ¼ppel-like factor 2 (KLF2) confers anti-inflammatory properties to endothelial cells through inhibition of activator protein 1, presumably by interfering with MAPK cascades. To gain insight into the regulation of these cascades by KLF2, we used antibody arrays in combination with time-course mRNA micro-array analysis. No gross changes in MAPKs were detected, rather phosphorylation of actin cytoskeleton-associated proteins, including Focal Adhesion Kinase, was markedly repressed by KLF2. Furthermore, we demonstrate that KLF2-mediated inhibition of Jun NH2-terminal kinase (JNK) and its downstream targets ATF2/c-Jun is dependent on the cytoskeleton. Specifically, KLF2 directs the formation of typical short basal actin filaments, we term shear fibers, which are distinct from thrombin- or TNF-Î±-induced stress fibers. KLF2 is shown to be essential for shear stress-induced cell alignment, concomitant shear fiber assembly and inhibition of JNK signaling. These findings link the specific effects of shear-induced KLF2 on endothelial morphology to the suppression of JNK MAPK signaling in vascular homeostasis via novel actin shear fibers. Tramscriptome profiling: Three independent isolates of Human Umbilical Vein Endothelial cells were transduced with lentiviral vectors expressing Kruppel Like Factor 2 (KLF2) or no protein (mock), and at time after transduction 24 h, 48 h, 72 h , RNA was isolated and hybridized to GPL4868 microarrays using dye swap procedure Kinome profiling: Two independent isolates of Human Umbilical Vein Endothelial cells were transduced with lentiviral vectors expressing Kruppel Like Factor 2 (KLF2) or no protein (mock), and at time after transduction 72 h , total cellular protein was isolated and hybridized to Kinexus KAM-1.1 phosphoprotein (kinexus) microarrays using dual color procedure in duplicate

2010-06-25 | E-GEOD-19412 | biostudies-arrayexpress

KLF2-induced actin shear fibers control both alignment to flow and JNK signaling in vascular endothelium

Project description:The shear stress-induced transcription factor Krüppel-like factor 2 (KLF2) confers anti-inflammatory properties to endothelial cells through inhibition of activator protein 1, presumably by interfering with MAPK cascades. To gain insight into the regulation of these cascades by KLF2, we used antibody arrays in combination with time-course mRNA micro-array analysis. No gross changes in MAPKs were detected, rather phosphorylation of actin cytoskeleton-associated proteins, including Focal Adhesion Kinase, was markedly repressed by KLF2. Furthermore, we demonstrate that KLF2-mediated inhibition of Jun NH2-terminal kinase (JNK) and its downstream targets ATF2/c-Jun is dependent on the cytoskeleton. Specifically, KLF2 directs the formation of typical short basal actin filaments, we term shear fibers, which are distinct from thrombin- or TNF-α-induced stress fibers. KLF2 is shown to be essential for shear stress-induced cell alignment, concomitant shear fiber assembly and inhibition of JNK signaling. These findings link the specific effects of shear-induced KLF2 on endothelial morphology to the suppression of JNK MAPK signaling in vascular homeostasis via novel actin shear fibers.

2009-12-11 | GSE19412 | GEO

Neuron-Specific Fluorescence Reporter-Based Live Cell Tracing for Transdifferentiation of Mesenchymal Stem Cells into Neurons by Chemical Compound.

Project description:Although transdifferentiation of mesenchymal stem cells (MSCs) into neurons increases the possibility of therapeutic use of MSCs for neurodevelopmental disorders, the use of MSCs has the limitation on differentiation efficiency to neuronal lineage and lack of an easy method to monitor the transdifferentiation. In this study, using time-lapse live cell imaging, we assessed the neuronal differentiation of MSCs induced by a small molecule "NHPDQC (N-hydroxy-2-oxo-3-(3-phenylprophyl)-1,2-dihydroquinoxaline-6-carboxamide, C18H17N3O3)." Plasmid vector containing red fluorescence reporter genes under the control of the tubulin α1 (Tα1) promoter (pTα1-DsRed2) traced the neuronal differentiation of MSCs. Two days after NHPDQC treatment, MSCs showed neuron-like phenotype with neurite outgrowth and high expression of neuron-specific markers in more than 95% cells. The fluorescence signals increased in the cytoplasm of pTα1-DsRed2-transfected MSCs after NHPDQC treatment. In vitro monitoring of MSCs along the time courses showed progressive increase of fluorescence till 30 h after treatment, corresponding with the increase in neurite length. We examined an efficient neuronal differentiation of MSCs by NHPDQC alone and monitored the temporal changes of neuronal differentiation by neuron-specific fluorescence reporter along time. This method would help further our understanding of the differentiation of MSCs to produce neurons by simple treatment of small molecule.

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