Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1290527 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:9 samples from biofilter packing Raw sequence reads
| PRJNA450592 | ENA
Project description:The organization of chromatin, governed by physicochemical interactions, nucleosome positioning, and histone modifications, regulates transcription to influence cellular plasticity and cell fate. We explored whether the organization of chromatin into nanoscale packing domains is involved in regulating transcriptional programs that govern stemness and responses to chemotherapy. Specifically, chromatin packing domains are a unit of chromatin structure at the single-cell level playing a critical role in regulating cellular transcriptional plasticity and access to the transcriptional landscape. Using an optical spectroscopic nanosensing technology, partial wave spectroscopic (PWS) microscopy, we show that ovarian cancer-derived cancer stem cells (CSCs) display upregulation of nanoscale chromatin packing domains (P<0.05) compared to non-CSCs cells. CUT&Tag sequencing with antibodies for repressive H3K27me3 and active H3K4me3 and H3K27ac marks identified 4438 H3K27me3 differentially enriched regions (P<0.05), of which 2786 were detected in CSCs, supporting chromatin packing domain upregulation in ovarian CSCs. Additionally, more poised genes with both H3K4me3 and H3K27me3 marks were identified in CSCs (n=2292) vs. non-CSCs (n=932), supporting the increased transcriptional plasticity of CSCs. Corresponding to the distinct organization of chromatin marks in CSCs, comparative transcriptomic analyses yielded a higher intercellular transcriptional heterogeneity in global gene expression at baseline in CSCs vs. non-CSCs. In response to cisplatin, genes with low baseline expression levels underwent the highest upregulation in CSCs, demonstrating transcriptional plasticity under the stress of chemotherapy. Treatment of CSCs with epigenome targeting drugs downregulating chromatin packing domain formation promoted cellular differentiation. In particular, the Dot1L inhibitor (Dot1Li) downregulated chromatin domains and blocked transcriptional plasticity. This resulted in the reversal of stemness features and inhibition of tumor initiation capacity. The results support that CSCs harbor upregulated chromatin packing domains, contributing to transcriptional and cell plasticity that epigenome modifiers can target.
2025-03-18 | GSE268062 | GEO
Project description:In single cells, variably sized nanoscale chromatin structures are observed but it is unknown if these form a cohesive framework that regulates RNA transcription. Herein we demonstrate that the human genome is an emergent, self-assembling system. Conformationally-defined heterogenous, nanoscopic packing domains form by the interplay of transcription, nucleosome remodeling, and loop extrusion. We show that packing domains are not topologically associated domains. Instead, packing domains exist across a structure-function life-cycle that couples heterochromatin and transcription in situ, explaining how heterochromatin enzyme inhibition can produce a paradoxical decrease in transcription by destabilizing domain cores. Applied to development and aging, we show the pairing of heterochromatin and transcription at myogenic genes that could be disrupted by nuclear swelling. In sum, packing domains represent a new foundation to explore the interactions of chromatin and transcription at the single cell level in human health.
2024-12-06 | GSE283236 | GEO
Project description:The organization of chromatin, governed by physicochemical interactions, nucleosome positioning, and histone modifications, regulates transcription to influence cellular plasticity and cell fate. We explored whether the organization of chromatin into nanoscale packing domains is involved in regulating transcriptional programs that govern stemness and responses to chemotherapy. Specifically, chromatin packing domains are a unit of chromatin structure at the single-cell level playing a critical role in regulating cellular transcriptional plasticity and access to the transcriptional landscape. Using an optical spectroscopic nanosensing technology, partial wave spectroscopic (PWS) microscopy, we show that ovarian cancer-derived cancer stem cells (CSCs) display upregulation of nanoscale chromatin packing domains (P<0.05) compared to non-CSCs cells. CUT&Tag sequencing with antibodies for repressive H3K27me3 and active H3K4me3 and H3K27ac marks identified 4438 H3K27me3 differentially enriched regions (P<0.05), of which 2786 were detected in CSCs, supporting chromatin packing domain upregulation in ovarian CSCs. Additionally, more poised genes with both H3K4me3 and H3K27me3 marks were identified in CSCs (n=2292) vs. non-CSCs (n=932), supporting the increased transcriptional plasticity of CSCs. Corresponding to the distinct organization of chromatin marks in CSCs, comparative transcriptomic analyses yielded a higher intercellular transcriptional heterogeneity in global gene expression at baseline in CSCs vs. non-CSCs. In response to cisplatin, genes with low baseline expression levels underwent the highest upregulation in CSCs, demonstrating transcriptional plasticity under the stress of chemotherapy. Treatment of CSCs with epigenome targeting drugs downregulating chromatin packing domain formation promoted cellular differentiation. In particular, the Dot1L inhibitor (Dot1Li) downregulated chromatin domains and blocked transcriptional plasticity. This resulted in the reversal of stemness features and inhibition of tumor initiation capacity. The results support that CSCs harbor upregulated chromatin packing domains, contributing to transcriptional and cell plasticity that epigenome modifiers can target.
2025-03-18 | GSE268061 | GEO
Project description:The organization of chromatin, governed by physicochemical interactions, nucleosome positioning, and histone modifications, regulates transcription to influence cellular plasticity and cell fate. We explored whether the organization of chromatin into nanoscale packing domains is involved in regulating transcriptional programs that govern stemness and responses to chemotherapy. Specifically, chromatin packing domains are a unit of chromatin structure at the single-cell level playing a critical role in regulating cellular transcriptional plasticity and access to the transcriptional landscape. Using an optical spectroscopic nanosensing technology, partial wave spectroscopic (PWS) microscopy, we show that ovarian cancer-derived cancer stem cells (CSCs) display upregulation of nanoscale chromatin packing domains (P<0.05) compared to non-CSCs cells. CUT&Tag sequencing with antibodies for repressive H3K27me3 and active H3K4me3 and H3K27ac marks identified 4438 H3K27me3 differentially enriched regions (P<0.05), of which 2786 were detected in CSCs, supporting chromatin packing domain upregulation in ovarian CSCs. Additionally, more poised genes with both H3K4me3 and H3K27me3 marks were identified in CSCs (n=2292) vs. non-CSCs (n=932), supporting the increased transcriptional plasticity of CSCs. Corresponding to the distinct organization of chromatin marks in CSCs, comparative transcriptomic analyses yielded a higher intercellular transcriptional heterogeneity in global gene expression at baseline in CSCs vs. non-CSCs. In response to cisplatin, genes with low baseline expression levels underwent the highest upregulation in CSCs, demonstrating transcriptional plasticity under the stress of chemotherapy. Treatment of CSCs with epigenome targeting drugs downregulating chromatin packing domain formation promoted cellular differentiation. In particular, the Dot1L inhibitor (Dot1Li) downregulated chromatin domains and blocked transcriptional plasticity. This resulted in the reversal of stemness features and inhibition of tumor initiation capacity. The results support that CSCs harbor upregulated chromatin packing domains, contributing to transcriptional and cell plasticity that epigenome modifiers can target.
2025-03-18 | GSE268060 | GEO
Project description:Biofilter-release
| PRJEB78888 | ENA