Expression data from mouse embryo (E5) cultured in the narrow and wide cavity
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE51198 | GEO | 2013/09/27
SECONDARY ACCESSION(S): PRJNA221580
REPOSITORIES: GEO
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Project description:The mouse anterior-posterior (A-P) axis polarization is preceded by formation of the distal visceral endoderm (DVE). However, the mechanism of the emergence of DVE cells is not well understood. Here, we show by in vitro culturing of embryos immediately after implantation in micro-fabricated cavities (narrow; 90 micro-meter, wide; 180 miro-meter in diameter) that the external mechanical cues exerted on the embryo, i.e. cultured in the narrow cavity, are crucial for DVE formation as well as elongated egg cylinder shape. This implies that these developmental events immediately after implantation are not simply embryo-autonomous processes but require extrinsic mechanical factors. Further whole genome-wide gene expression profiles with DNA microarray revealed that no significant difference of transcripts were evident with or without mechanical cues except DVE-related markers. Thus, we propose that external mechanical cues rather than not specific molecular pathways can trigger the establishment of the A-P axis polarization, which is one of the fundamental proccesses of mammalian embryogenesis. To identify the differences between the embryos cultured with or without external mechanical cues, we collected mouse embryos at E5.0 and cultured in the narrow (90 micro-meter in diameter) or the wide (180 micro-meter in diameter) cavities for 8 hours for RNA extraction and hybridization on Affymetrix microarrays. Arrays were performed using Affymetrix mouse Gene 1.0 ST arrays. Analysis was performed on three biological replicates of the mouse embryos cultured in the narrow and wide cavities for 8 hours.
2013-09-27 | E-GEOD-51198 | biostudies-arrayexpress
Project description:The extracellular matrix (ECM) is fundamental to cellular and tissue structural integrity and provides mechanical cues to initiate diverse biological functions1. The quality and quantity of ECM determines tissue stiffness and controls gene expression, cell fate, and cell cycle progression in various cell types. ECM-cell interactions are mediated by focal adhesions (FAs), the main hub for mechanotransduction, connecting ECM, integrins and cytoskeleton. In the blood vessels, an additional layer of mechanical cues derived from pulsatile blood flow and pressure play a pivotal role in homeostasis and disease development. However, how cells sense and integrate different mechanical cues to maintain the blood vessel wall is largely unknown. Vascular ECM is synthesized by SMCs from mid-gestation to early postnatal period and determines the material and mechanical properties of the blood vessels14. Owing to the long half-life of ECM, blood vessels are generally thought to stand life-long mechanical stress without regeneration, particularly in large arteries. However, it is not completely known whether local micro-remodeling system exists for the maintenance of the vessel wall. To search for a potential remodeling factor(s), we performed cyclic stretch experiments (1 Hz; 20% strain) using rat vascular SMCs for 20 hours (h) with or without Brefeldin A (BFA), a protein transporter inhibitor. Conditioned media (CM) were analyzed using quantitative mass spectrometry.
2020-03-18 | PXD013915 | JPOST Repository
Project description:Rhythmic growth explained by coincidence between internal and external cues
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Project description:The special AT-rich sequence-binding (SATB) protein DVE-1 is widely recognized for its pivotal involvement in orchestrating the retrograde mitochondrial unfolded protein response (mitoUPR) in C. elegans. In our study of downstream factors contributing to lifespan extension in sensory ciliary mutants, we find that DVE-1 is crucial for this longevity effect independent of its canonical mitoUPR function. Additionally, DVE-1 also influences lifespan under conditions of dietary restriction and germline loss, again distinct from its role in mitoUPR. Mechanistically, while mitochondrial stress typically prompts nuclear accumulation of DVE-1 to initiate the transcriptional mitoUPR program, these long-lived mutants reduce DVE-1 nuclear accumulation, likely by enhancing its cytosolic translocation. This observation suggests a cytosolic role for DVE-1 in lifespan extension. Overall, our study implies that, in contrast to the more narrowly defined role of the mitoUPR-related transcription factor ATFS-1, DVE-1 may possess broader functions than previously recognized in modulating longevity and defending against stress.
2024-09-27 | GSE276887 | GEO
Project description:Phenotype switching is a form of cellular plasticity in which cancer cells reversibly move between two opposite extremes - proliferative versus invasive states. While it has long been hypothesised that such switching is triggered by external cues, the identity of these cues has remained elusive. Here, we demonstrate that mechanical confinement mediates phenotype switching through chromatin remodelling. Using a zebrafish model of melanoma coupled with human samples, we profiled tumour cells at the interface between the tumour and surrounding microenvironment. Morphological analysis of these rare cells showed flattened, elliptical nuclei suggestive of mechanical confinement by nearby adjacent tissue. Spatial and single-cell transcriptomics demonstrated that the interface cells adopted a gene program of neuronal invasion, including acquisition of an acetylated tubulin cage that protects the nucleus during migration. We identified the DNA-bending protein HMGB2 as a confinement-induced mediator of the neuronal state. HMGB2 is upregulated in confined cells, and quantitative modelling revealed that confinement prolongs contact time between HMGB2 and chromatin, leading to changes in chromatin configuration that favour the neuronal phenotype. Genetic disruption of HMGB2 showed that it regulates the trade-off between proliferative and invasive states, in which confined HMGB2high tumour cells are less proliferative but more drug resistant. Our results implicate the mechanical microenvironment as a mechanism for phenotype switching in melanoma.
2024-01-24 | GSE253802 | GEO
Project description:Phenotype switching is a form of cellular plasticity in which cancer cells reversibly move between two opposite extremes - proliferative versus invasive states. While it has long been hypothesised that such switching is triggered by external cues, the identity of these cues has remained elusive. Here, we demonstrate that mechanical confinement mediates phenotype switching through chromatin remodelling. Using a zebrafish model of melanoma coupled with human samples, we profiled tumour cells at the interface between the tumour and surrounding microenvironment. Morphological analysis of these rare cells showed flattened, elliptical nuclei suggestive of mechanical confinement by nearby adjacent tissue. Spatial and single-cell transcriptomics demonstrated that the interface cells adopted a gene program of neuronal invasion, including acquisition of an acetylated tubulin cage that protects the nucleus during migration. We identified the DNA-bending protein HMGB2 as a confinement-induced mediator of the neuronal state. HMGB2 is upregulated in confined cells, and quantitative modelling revealed that confinement prolongs contact time between HMGB2 and chromatin, leading to changes in chromatin configuration that favour the neuronal phenotype. Genetic disruption of HMGB2 showed that it regulates the trade-off between proliferative and invasive states, in which confined HMGB2high tumour cells are less proliferative but more drug resistant. Our results implicate the mechanical microenvironment as a mechanism for phenotype switching in melanoma.
2024-01-24 | GSE253801 | GEO
Project description:Phenotype switching is a form of cellular plasticity in which cancer cells reversibly move between two opposite extremes - proliferative versus invasive states. While it has long been hypothesised that such switching is triggered by external cues, the identity of these cues has remained elusive. Here, we demonstrate that mechanical confinement mediates phenotype switching through chromatin remodelling. Using a zebrafish model of melanoma coupled with human samples, we profiled tumour cells at the interface between the tumour and surrounding microenvironment. Morphological analysis of these rare cells showed flattened, elliptical nuclei suggestive of mechanical confinement by nearby adjacent tissue. Spatial and single-cell transcriptomics demonstrated that the interface cells adopted a gene program of neuronal invasion, including acquisition of an acetylated tubulin cage that protects the nucleus during migration. We identified the DNA-bending protein HMGB2 as a confinement-induced mediator of the neuronal state. HMGB2 is upregulated in confined cells, and quantitative modelling revealed that confinement prolongs contact time between HMGB2 and chromatin, leading to changes in chromatin configuration that favour the neuronal phenotype. Genetic disruption of HMGB2 showed that it regulates the trade-off between proliferative and invasive states, in which confined HMGB2high tumour cells are less proliferative but more drug resistant. Our results implicate the mechanical microenvironment as a mechanism for phenotype switching in melanoma.
2024-01-24 | GSE253800 | GEO
Project description:modENCODE_submission_4804 This submission comes from a modENCODE project of Michael Snyder. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We are identifying the DNA binding sites for 300 transcription factors in C. elegans. Each transcription factor gene is tagged with the same GFP fusion protein, permitting validation of the gene's correct spatio-temporal expression pattern in transgenic animals. Chromatin immunoprecipitation on each strain is peformed using an anti-GFP antibody, and any bound DNA is deep-sequenced using Solexa GA2 technology. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-seq. BIOLOGICAL SOURCE: Strain: OP398(official name : OP398 genotype : unc-119(ed3) III; wgIs398(dve-1::TY1EGFPFLAG C;unc-119(+)) outcross : 3 mutagen : Bombard tags : GFP::3xFlag description : This strain's transgene was constructed by Mihail Sarov at the Max Planck Institute for Cell Biology and Genetics in Dresden description : using Tony Hyman's recombineering pipeline. The resulting plasmid was used for biolistic transformation of an unc-119(ed3) strain. The DVE-1::EGFP fusion protein is expressed in the correct dve-1 spatio-temporal expression pattern. This strain was used for ChIP-seq experiments to map the in vivo binding sites for the DVE-1 transcription factor. made_by : Unknown ); Developmental Stage: Late Embryo; Genotype: unc-119(ed3) III; wgIs398(dve-1::TY1EGFPFLAG C;unc-119(+)); Sex: Hermaphrodite; EXPERIMENTAL FACTORS: Developmental Stage Late Embryo; Target gene dve-1; Strain OP398(official name : OP398 genotype : unc-119(ed3) III; wgIs398(dve-1::TY1EGFPFLAG C;unc-119(+)) outcross : 3 mutagen : Bombard tags : GFP::3xFlag description : This strain's transgene was constructed by Mihail Sarov at the Max Planck Institute for Cell Biology and Genetics in Dresden description : using Tony Hyman's recombineering pipeline. The resulting plasmid was used for biolistic transformation of an unc-119(ed3) strain. The DVE-1::EGFP fusion protein is expressed in the correct dve-1 spatio-temporal expression pattern. This strain was used for ChIP-seq experiments to map the in vivo binding sites for the DVE-1 transcription factor. made_by : Unknown ); temp (temperature) 20 degree celsius
2013-07-11 | E-GEOD-48749 | biostudies-arrayexpress
Project description:modENCODE_submission_4803 This submission comes from a modENCODE project of Michael Snyder. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We are identifying the DNA binding sites for 300 transcription factors in C. elegans. Each transcription factor gene is tagged with the same GFP fusion protein, permitting validation of the gene's correct spatio-temporal expression pattern in transgenic animals. Chromatin immunoprecipitation on each strain is peformed using an anti-GFP antibody, and any bound DNA is deep-sequenced using Solexa GA2 technology. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-seq. BIOLOGICAL SOURCE: Strain: OP398(official name : OP398 genotype : unc-119(ed3) III; wgIs398(dve-1::TY1EGFPFLAG C;unc-119(+)) outcross : 3 mutagen : Bombard tags : GFP::3xFlag description : This strain's transgene was constructed by Mihail Sarov at the Max Planck Institute for Cell Biology and Genetics in Dresden description : using Tony Hyman's recombineering pipeline. The resulting plasmid was used for biolistic transformation of an unc-119(ed3) strain. The DVE-1::EGFP fusion protein is expressed in the correct dve-1 spatio-temporal expression pattern. This strain was used for ChIP-seq experiments to map the in vivo binding sites for the DVE-1 transcription factor. made_by : Unknown ); Developmental Stage: L4; Genotype: unc-119(ed3) III; wgIs398(dve-1::TY1EGFPFLAG C;unc-119(+)); Sex: Hermaphrodite; EXPERIMENTAL FACTORS: Developmental Stage L4; Target gene dve-1; Strain OP398(official name : OP398 genotype : unc-119(ed3) III; wgIs398(dve-1::TY1EGFPFLAG C;unc-119(+)) outcross : 3 mutagen : Bombard tags : GFP::3xFlag description : This strain's transgene was constructed by Mihail Sarov at the Max Planck Institute for Cell Biology and Genetics in Dresden description : using Tony Hyman's recombineering pipeline. The resulting plasmid was used for biolistic transformation of an unc-119(ed3) strain. The DVE-1::EGFP fusion protein is expressed in the correct dve-1 spatio-temporal expression pattern. This strain was used for ChIP-seq experiments to map the in vivo binding sites for the DVE-1 transcription factor. made_by : Unknown ); temp (temperature) 20 degree celsius
2013-07-11 | E-GEOD-48748 | biostudies-arrayexpress
Project description:It is not understood, how mechanical signals influence the behavior and action of circulating cells in our body. Previous studies showed that the process of migration through narrow slits might enhance lifespan of polymorpho-nuclear cells (PMN / neutrophil). But it is unknown, how the mechanical signal is received, relayed, and translated into specific phenotype shift in PMN. Here we investigated whether compressional force affects defense system of circulating lymphocytes by increasing their killing ability during migration through narrow endothelial junctions. To decipher the receiving and transducing components of this mechanical signal relay process, we performed gene expression analysis between transmigrated and non-transmigrated neutrophils. Comparison of early gene-expression pattern of transmigrated and non-transmigrated neutrophils revealed a huge change in gene expression profile. Molecular and genetic analysis of the proteins revealed from gene-expression analysis led us to understand the mechanism of mechanical signal relay from the neutrophil membrane to bacterial-killing machinery. As neutrophils are most abundant and immediate-responding circulating immune cells in our body, our study advances the path for understanding the general process of mechano-transduction, and mechano-modulatory applications with mechanically enhanced neutrophils.
2023-12-04 | GSE210111 | GEO