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Viscoelastic Extracellular Matrix Enhances Epigenetic Remodeling and Cellular Plasticity [ATAC-seq]

ABSTRACT: Viscoelastic Extracellular Matrix Enhances Epigenetic Remodeling and Cellular Plasticity [ATAC-seq]

PROVIDER: PRJNA1244332 | ENA |

REPOSITORIES: ENA

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Viscoelastic Extracellular Matrix Enhances Epigenetic Remodeling and Cellular Plasticity

Project description:Viscoelastic Extracellular Matrix Enhances Epigenetic Remodeling and Cellular Plasticity

| PRJNA1244329 | ENA

Viscoelastic Extracellular Matrix Enhances Epigenetic Remodeling and Cellular Plasticity [RNA-seq]

Project description:Viscoelastic Extracellular Matrix Enhances Epigenetic Remodeling and Cellular Plasticity [RNA-seq]

| PRJNA1244331 | ENA

Viscoelastic Extracellular Matrix Enhances Epigenetic Remodeling and Cellular Plasticity [RNA-seq]

Project description:Extracellular matrices of living tissues exhibit viscoelastic properties, yet how these properties regulate chromatin and the epigenome remains unclear. Here, we show that viscoelastic substrates induce changes in nuclear architecture and epigenome, with more pronounced effects on softer surfaces. Fibroblasts on viscoelastic substrates display larger nuclei, lower chromatin compaction, and differential expression of distinct sets of genes related to the cytoskeleton and nuclear function compared to those on purely elastic surfaces. Slow-relaxing viscoelastic substrates reduce lamin A/C expression and enhance nuclear remodeling. These structural changes are accompanied by a global increase in euchromatin marks and local increase in chromatin accessibility at cis-regulatory elements associated with neuronal and pluripotent genes. Consequently, viscoelastic substrates improve the reprogramming efficiency from fibroblasts into neurons and induced pluripotent stem cells. Collectively, our findings unravel the roles of matrix viscoelasticity in epigenetic regulation and cell reprogramming, with implications for designing smart materials for cell fate engineering.

2025-04-02 | GSE293383 | GEO

Viscoelastic Extracellular Matrix Enhances Epigenetic Remodeling and Cellular Plasticity [ATAC-seq]

2025-04-02 | GSE293382 | GEO

Viscoelastic Extracellular Matrix Enhances Epigenetic Remodeling and Cellular Plasticity

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-04-02 | GSE293384 | GEO

Microglial remodeling of the extracellular matrix promotes synapse plasticity

Project description:Microglial remodeling of the extracellular matrix promotes synapse plasticity

| PRJNA633361 | ENA

Microglial remodeling of the extracellular matrix promotes synapse plasticity [Microglia]

Project description:Microglial remodeling of the extracellular matrix promotes synapse plasticity [Microglia]

| PRJNA633363 | ENA

Microglial remodeling of the extracellular matrix promotes synapse plasticity [Neuronal nuclei]

Project description:Microglial remodeling of the extracellular matrix promotes synapse plasticity [Neuronal nuclei]

| PRJNA633364 | ENA

Bromodomain inhibitor PFI-3 induces cellular plasticity and enhances iPSC reprogramming efficiency by targeting extracellular matrix

Project description:Bromodomain inhibitor PFI-3 induces cellular plasticity and enhances iPSC reprogramming efficiency by targeting extracellular matrix

| PRJNA1008157 | ENA

Extracellular Matrix Formation Enhances the Ability of Streptococcus pneumoniae to Cause Invasive Disease

Project description:Background. During infection, pneumococci exist mainly in sessile biofilms rather than in planktonic form, except during sepsis. However, relatively little is known about how biofilms contribute to pneumococcal pathogenesis. Methods. We performed a biofilm assay and mouse infection experiments on opaque and transparent variants of a clinical serotype 19F strain. Results. After 4 days incubation, scanning electron microscopy revealed that opaque biofilm bacteria produced an extracellular matrix, whereas the transparent variant did not. The opaque biofilm-derived bacteria translocated from the nasopharynx to the lungs and brain of mice, and showed 100-fold greater in vitro adherence to A549 cells. Microarray analysis of planktonic and sessile bacteria from transparent and opaque variants showed differential gene expression in two operons: the lic operon, involved in choline uptake, and in the two-component system, ciaRH. Mutants of these genes did not form an extracellular matrix, could not translocate from the nasopharynx to the lungs or the brain, and adhered poorly to A549 cells. Conclusions. We conclude that only the opaque phenotype is able to form extracellular matrix, and that the lic operon and ciaRH contribute to this process. We propose that during infection, extracellular matrix formation enhances the ability of pneumococci to cause invasive disease. Data is also available from http://bugs.sgul.ac.uk/E-BUGS-117

2011-04-20 | E-BUGS-117 | biostudies-arrayexpress

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