Tissue confinement regulates cell growth and size in epithelia
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA947259 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23934059_1.fastq.gz | Fastqsanger.gz | |||
| SRR23934059_2.fastq.gz | Fastqsanger.gz | |||
| SRR23934060_1.fastq.gz | Fastqsanger.gz | |||
| SRR23934060_2.fastq.gz | Fastqsanger.gz | |||
| SRR23934061_1.fastq.gz | Fastqsanger.gz |
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Project description:Cell proliferation is a central process in tissue development, homeostasis and disease. Yet how proliferation is regulated in the tissue context remains poorly understood. Here, we introduce a quantitative framework to elucidate how tissue growth dynamics regulate cell proliferation. We show that a limiting rate of tissue expansion creates confinement that suppresses cell growth; however, this confinement does not directly affect the cell cycle. This leads to uncoupling between rates of cell growth and division in epithelia and, thereby, reduces cell volume. Division becomes arrested at a minimal cell volume, which is consistent across diverse epithelia in vivo. Here, the nucleus approaches the minimum volume capable of packaging the genome. The loss of Cyclin D1-dependent cell volume regulation results in an abnormally high nuclear-to-cytoplasmic volume ratio and DNA damage. Overall, we demonstrate how epithelial proliferation is regulated by the interplay between tissue confinement and cell volume regulation.
2023-05-31 | GSE227906 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE25440: Individual variation in confinement response at 168h GSE25473: Time course study of confinement stress in HR and LR trout lines Refer to individual Series
2010-11-24 | E-GEOD-25584 | biostudies-arrayexpress
Project description:Farmed fish are unavoidably exposed to husbandry-related stressors which can result in outbreaks of disease, reduced reproductive success and poor growth. Biomarkers are needed for the establishment of selective breeding approaches for the production of stress resistant fish. In this context, microarray analysis has been carried out on liver tissues of two genetic lines of rainbow trout, high responders (HR) and low responders (LR), after confinement for various time periods. Microarray hybridisations provided gene expression profiles for pools of fish (stress: n=5; control: n=3) after 6h, 24h and 168h of confinement stress. Keywords : stress response, pools, time course, comparison of two lines. Samples were hybridised directly to each other in a parallel loop design. Each treatment (LC, LS, HC, HS) was hybidised in a loop of all 3 time points and each treatment loop was interconnected by hybridisations at a specific time. The publication will have this figure.
2010-11-24 | E-GEOD-25473 | biostudies-arrayexpress
Project description:The effects of short-term confinement on gene expression profiles in blood were evaluated. Fourteen days confinement study was conducted 2 times. In each experiment, 8 male subjects were stayed in an isolation and confinement facility at Japan Aerospace Exploration Agency. DNA microarray of extracted RNA from whole blood samples revealed that the expression levels of 3,659 genes were significantly altered by the 14-day confinement. The changes in gene expression profiles were not exactly the same as those in response to the other stress conditions, such as chronic psychological stress and spaceflight. In particular, 7 genes, LIN9, AK125040.1, MGC45922, C9orf173-AS1, OR1P1P, KRTAP10-12, and ARFRP1, responded to the confinement prominently. Therefore, the analysis of expression levels of these genes might be useful to assess the stress responses of human body to the confinement. In addition, biological interpretation of the alteration of gene expression profiles with Ingenuity Pathway Analysis indicated that 14-day confinement stimulated various signaling related to proinflammation and leukocyte extravasation but suppressed apoptosis signaling. In agreement with the interpretation, the decrease of white blood cells in blood was confirmed during the confinement. On the other hand, red blood cells and platelets did not decrease. These results suggest that 14-day confinement is likely to induce shift of white blood cells from “the circulating pool” to “the marginated pool”.
2022-10-18 | GSE103605 | GEO
Project description:Farmed fish are unavoidably exposed to husbandry-related stressors which can result in outbreaks of disease, reduced reproductive success and poor growth. Biomarkers are needed for the establishment of selective breeding approaches for the production of stress resistant fish. In this context, microarray analysis has been carried out on liver tissues of two genetic lines of rainbow trout, high responders (HR) and low responders (LR), after confinement for various time periods. Microarray hybridisations provided gene expression profiles for pools of fish (stress: n=5; control: n=3) after 6h, 24h and 168h of confinement stress. Keywords : stress response, pools, time course, comparison of two lines.
2010-11-24 | GSE25473 | GEO
Project description:Farmed fish are unavoidably exposed to husbandry-related stressors which can result in outbreaks of disease, reduced reproductive success and poor growth. Biomarkers are needed for the establishment of selective breeding approaches for the production of stress resistant fish. In this context, microarray analysis has been carried out on liver tissues of two genetic lines of rainbow trout, high responders (HR) and low responders (LR), after confinement for various time periods. Microarray hybridisations provided gene expression profiles for 10 individual fish (5 of the HR line and 5 of the LR line) after 168h of confinment stress. Keywords : stress response, individual variation, fixed time point, comparison of two lines All 10 samples were hybridised against a common reference source that contained equal amounts of all 10 samples. Each sample was hybridised twice against this reference using a dye-swap setup.
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Project description:How cells control the overall size of membrane-bound organelles is an important unanswered question of cell biology. Fission yeast cells maintain a nuclear size that is proportional to cellular size, resulting in a constant ratio between the nuclear and cellular volumes (N/C ratio). To shed light on nuclear size control we conducted a genome-wide visual screen of a fission yeast gene deletion collection for mutants altered in their N/C ratio, and found that defects in both nucleocytoplasmic mRNA transport and nuclear membrane proliferation alter the N/C ratio. Perturbing nuclear mRNA export causes general bulk accumulation of both mRNA and protein, and a N/C ratio increase which is dependent on new membrane synthesis. Dysregulation of nuclear membrane growth also results in an enlarged N/C ratio, and additionally generates an aberrant nuclear shape. We propose that both properly regulated nucleocytoplasmic transport and nuclear membrane growth are central for controlling nuclear size.
2017-06-05 | PXD004530 | Pride
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.
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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