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Transcription induces context-dependent remodeling of chromatin architecture during differentiation

ABSTRACT: Transcription induces context-dependent remodeling of chromatin architecture during differentiation

PROVIDER: PRJNA902328 | ENA |

REPOSITORIES: ENA

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Transcription induces context-dependent remodeling of chromatin architecture during differentiation

Project description:Metazoan chromosomes are organized into discrete domains (TADs), believed to contribute to the regulation of transcriptional programs. Despite extensive correlation between TAD organization and gene activity, a direct mechanistic link is unclear, with perturbation studies often showing little effect. To follow TAD dynamics during development, we used Capture Hi-C to interrogate the TADs around key differentially expressed genes during mouse thymocyte maturation, uncovering specific remodeling events. Notably, one TAD boundary was broadened to accommodate RNA polymerase elongation past the border, and sub-domains were formed around some activated genes without changes in CTCF binding. The ectopic induction of one gene was sufficient to recapitulate microdomain formation in embryonic stem cells, providing strong evidence that transcription can directly remodel chromatin structure. These results suggest that transcriptional processes drive complex, but non-universal, chromosome folding patterns that can be important in certain genomic contexts.

2023-10-26 | GSE218090 | GEO

Angioplasty induces epigenomic remodeling in injured arteries

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An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [memory + KrasG12D scRNA-seq]

Project description:An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [memory + KrasG12D scRNA-seq]

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Project description:An Epigenetic Memory of Inflammation Induces Context-Dependent Lineage Plasticity in the Pancreas with Divergent Phenotypic Outcomes [Acute Pancreatitis scRNA-seq]

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The chromatin remodeling enzyme Chd4 regulates genome architecture in the mouse brain

Project description:The development and function of the brain require tight control of gene expression. Genome architecture is thought to play a critical regulatory role in gene expression, but the mechanisms governing genome architecture in the brain in vivo remain poorly understood. Here, we report that conditional knockout of the chromatin remodeling enzyme Chd4 in granule neurons of the mouse cerebellum increases accessibility of gene regulatory sites genome-wide in vivo. Conditional knockout of Chd4 promotes recruitment of the architectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo. Importantly, in vivo profiling of genome architecture reveals that conditional knockout of Chd4 strengthens interactions among developmentally repressed contact domains as well as genomic loops in a manner that tightly correlates with increased accessibility, enhancer activity, and cohesin occupancy at these sites. Collectively, our findings define a role for chromatin remodeling in the control of genome architecture organization in the mammalian brain.

2020-04-13 | GSE138822 | GEO

Social reprogramming in ants induces longevity-associated glia remodeling

Project description:Social reprogramming in ants induces longevity-associated glia remodeling

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Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling

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Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programs

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A single dose of Ultraviolet-A induces proteome remodeling and senescence in primary human keratinocytes

Project description:The UVB component of the sunlight (290-320 nm) plays an important role in carcinogenesis through generation of high levels of bipyrimidine DNA photoproducts, while UVA (320-400 nm) has been associated with photoaging and tumor progression through generation of low, but continuous levels of DNA damage and oxidative stress. However, the contribution of UVA light to epidermal cell fate in the context of photoaging remains poorly understood. Here, by using proteomic analyses and biochemical assays for validation, we show that UVA induces proteome remodeling and senescence in primary keratinocytes, eliciting potent antioxidant and pro-inflammatory responses. As a model of early skin tumorigenesis during aging, immortalized non-malignant keratinocytes, bearing potentially oncogenic mutations and dysfunctional components of the senescent machinery , are resilient to UVA-induced stress, but are sensitive to paracrine oxidative stress and immune system activation induced by senescent neighboring keratinocytes. These observations reveal a new cellular mechanism by which UVA induces photoaging in the epidermis.

2022-02-17 | PXD025191 | Pride

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