Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transient loss of Polycomb components induces an epigenetic cancer fate

ABSTRACT: Transient loss of Polycomb components induces an epigenetic cancer fate

PROVIDER: PRJNA918577 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22984504_1.fastq.gz	Fastqsanger.gz
	SRR22984504_2.fastq.gz	Fastqsanger.gz
	SRR22984505_1.fastq.gz	Fastqsanger.gz
	SRR22984505_2.fastq.gz	Fastqsanger.gz
	SRR22984506_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 252

Similar Datasets

Transient loss of Polycomb components induces an epigenetic cancer fate

Project description:Although cancer initiation and progression are generally associated with the accumulation of somatic mutations, substantial epigenomic alterations underlie many aspects of tumorigenesis and cancer susceptibility, suggesting that genetic mechanisms might not be the only drivers of malignant transformation. However, whether purely non-genetic mechanisms are sufficient to initiate tumorigenesis irrespective of mutations is unknown. Here, we show that a transient perturbation of transcriptional silencing mediated by Polycomb Group proteins is sufficient to induce an irreversible switch to a cancer cell fate in Drosophila. This is linked to the irreversible derepression of genes that can drive tumorigenesis, including members of the JAK-STAT signaling pathway and zfh1, the fly homolog of the ZEB1 oncogene, whose aberrant activation is required for Polycomb-induced tumorigenesis. These data show that a reversible perturbation of Polycomb Group protein levels can induce cancer in the absence of driver mutations, suggesting that tumors can emerge through epigenetic dysregulation leading to inheritance of altered cell fates.

2024-02-28 | GSE222193 | GEO

Transient Polycomb activity represses developmental genes in growing oocytes.

Project description:Transient Polycomb activity represses developmental genes in growing oocytes.

| PRJNA796653 | ENA

Genome-wide mapping of Polycomb target genes unravels their roles in cell fate transitions

Project description:The Polycomb group (PcG) proteins form chromatin-modifying complexes that are essential for embryonic development and stem cell renewal and are commonly deregulated in cancer. Here, we identify their target genes using genome-wide location analysis in human embryonic fibroblasts. We find that Polycomb-Repressive Complex 1 (PRC1), PRC2, and tri-methylated histone H3K27 co-occupy >1000 silenced genes with a strong functional bias for embryonic development and cell fate decisions. We functionally identify 40 genes derepressed in human embryonic fibroblasts depleted of the PRC2 components (EZH2, EED, SUZ12) and the PRC1 component, BMI-1. Interestingly, several markers of osteogenesis, adipogenesis, and chrondrogenesis are among these genes, consistent with the mesenchymal origin of fibroblasts. Using a neuronal model of differentiation, we delineate two different mechanisms for regulating PcG target genes. For genes activated during differentiation, PcGs are displaced. However, for genes repressed during differentiation, we paradoxically find that they are already bound by the PcGs in nondifferentiated cells despite being actively transcribed. Our results are consistent with the hypothesis that PcGs are part of a preprogrammed memory system established during embryogenesis marking certain key genes for repressive signals during subsequent developmental and differentiation processes. Keywords: polycomb, development, differentiation, cell fate, stem cells, siRNA

2006-10-20 | GSE6015 | GEO

Polycomb Repressive Complex 2 Restricts Human Naive Pluripotent Stem Cell to Trophoblast Fate Induction

Project description:Human naive pluripotent stem cells have unrestricted lineage potential. Underpinning this property, naive cells are thought to lack chromatin-based lineage barriers. However, this assumption has not been tested. Here, we apply multi-omics to comprehensively define the chromatin-associated proteome, histone post-translational modifications and transcriptome of human naive and primed pluripotent stem cells. Integrating the chromatin-bound proteome and histone modification data sets reveals differences in the relative abundance and activities of distinct chromatin modules, identifying a strong enrichment of Polycomb Repressive Complex 2 (PRC2)-associated H3K27me3 in naive pluripotent stem cell chromatin. Single-cell approaches and human blastoid models reveal that PRC2 activity acts as a chromatin barrier restricting the differentiation of naive cells towards the trophoblast lineage, and inhibiting PRC2 promotes trophoblast fate induction and cavity formation. Our results establish that human naive pluripotent stem cells are not epigenetically unrestricted, but instead possess chromatin mechanisms that oppose the induction of alternative cell fates.

2022-05-06 | PXD028111 | Pride

Partial beta cell loss induces transient compensatory proliferation II

Project description:Partial beta cell loss induces transient compensatory proliferation II

| PRJNA1079820 | ENA

Partial beta cell loss induces transient compensatory proliferation I

Project description:Partial beta cell loss induces transient compensatory proliferation I

| PRJNA1079817 | ENA

Gene expression analysis of different subtypes of GSCs upon miR-128 overexpression or downregulation and after knockdown of Polycomb components BMI1 and SUZ12

Project description:To analyze the change of global transcriptome landscape among proneural and mesenchymal GSCs, after the transient knockdown of polycomb repressor complex and upon deregulations of miR-128 in different subtypes of GSCs

2017-04-30 | GSE89501 | GEO

Transient Hes5 activity instructs mesodermal cells toward a cardiac fate

Project description:Notch signaling plays a role in specifying a cardiac fate but the downstream effectors remain unknown. In this study we implicate the Notch downstream effector HES5 in cardiogenesis. We show transient Hes5 expression in early mesoderm of gastrulating embryos and demonstrate, by loss and gain-of-function experiments in mouse embryonic stem cells, that HES5 favors cardiac over primitive erythroid fate. Hes5 overexpression promotes upregulation of the cardiac gene Isl1, while the hematopoietic regulator Scl is downregulated. Moreover, whereas a pulse of Hes5 instructs cardiac commitment, sustained expression after lineage specification impairs progression of differentiation to contracting cardiomyocytes. These findings establish a role for HES5 in cardiogenesis and provide insights into the early cardiac molecular network.

2017-06-22 | GSE64540 | GEO

Core components of the nuclear pore bind distinct states of chromatin and contribute to Polycomb repression II

Project description:Interactions between the genome and the nuclear pore complex (NPC) have been implicated in multiple gene regulatory processes, but the underlying logic of these interactions remains poorly defined. Here, we report high-resolution chromatin binding maps of two core components of the NPC, Nup107 and Nup93, which reveal differential binding of these NPC subunits to active genes and Polycomb-covered silent regions, respectively. Comparison to Lamin-associated domains (LADs) revealed that NPC binding sites are often found within LADs, demonstrating a linear binding of the genome along the nuclear envelope. Significantly, we identified a functional role of Nup93 in silencing of Polycomb target genes and in spatial folding of Polycomb domains. Our findings lend to a model where nuclear pores bind different types of chromatin via interactions with specific core sub-complexes of the NPC, and the Nup93 sub-complex functions as a stabilizing scaffold for Polycomb domains.

2020-01-07 | GSE136115 | GEO

Core components of the nuclear pore bind distinct states of chromatin and contribute to Polycomb repression I

2020-01-07 | GSE135610 | GEO