The role of Polycomb in stem cell genome architecture

Mas, Glòria; Croce, Luciano Di

doi:10.1016/j.ceb.2016.09.006

Cited by 27 publications

(22 citation statements)

References 69 publications

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“…Finally, an enrichment for H3K27me3 histone mark associated with Polycomb Repressive Complexes is consistent with the independent findings of a very recent study in ES cells (Rhodes et al, 2020). Notably, the enrichment of Polycomb at the PIRs of cohesin-independent interactions appears to be considerably more pronounced in ES cells compared with differentiated cells such as HeLa (Rhodes et al, 2020), in line with the prominent role of these complexes in stem cell genome architecture and transcriptional control (Mas and Di Croce, 2016;Schoenfelder et al, 2015b).…”

Section: Discussionsupporting

confidence: 90%

Cohesin-dependent and independent mechanisms support chromosomal contacts between promoters and enhancers

Thiecke

Wutz

Muhar

et al. 2020

Preprint

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It is currently assumed that 3D chromosomal organisation plays a central role in transcriptional control. However, recent evidence shows that steady-state transcription of only a minority of genes is affected by depletion of architectural proteins such as cohesin and CTCF. Here, we have used Capture Hi-C to interrogate the dynamics of chromosomal contacts of all human gene promoters upon rapid architectural protein degradation. We show that promoter contacts lost in these conditions tend to be long-range, with at least one interaction partner localising in the vicinity of topologically associated domain (TAD) boundaries. In contrast, many shorter-range chromosomal contacts, particularly those that connect active promoters with each other and with active enhancers remain unaffected by cohesin and CTCF depletion. We demonstrate that the effects of cohesin depletion on nascent transcription can be explained by changes in the connectivity of their enhancers. Jointly, these results provide a mechanistic explanation to the limited, but consistent effects of cohesin and CTCF on steady-state transcription and point towards the existence of alternative enhancer-promoter pairing mechanisms that are independent of these proteins.

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Section: Discussionsupporting

confidence: 90%

Cohesin-dependent and independent mechanisms support chromosomal contacts between promoters and enhancers

Thiecke

Wutz

Muhar

et al. 2020

Preprint

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“…Polycomb Repressive Complex 2 (PRC2) drives trimethylation of histone 3 lysine 27 (H3K27me3), establishing gene silencing at developmentally-regulated loci. Conversely, trithorax group proteins, which mediate the trimethylation of histone 3 lysine 4 (H3K4me3), together with the histone lysine-specific demethylases, antagonize PRC2 repressive activity and allow gene expression in specific cell types [49]. In muscle stem cells, the absence of the repressive mark H3K27me3 across the genome and the concomitant existence of H3K4me3 at the transcription start sites maintain chromatin in a primed state, allowing cells to quickly respond to external stimuli [1].…”

Section: Introductionmentioning

confidence: 99%

Coordinated Actions of MicroRNAs with other Epigenetic Factors Regulate Skeletal Muscle Development and Adaptation

Bianchi

Renzini

Adamo

et al. 2017

IJMS

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Epigenetics plays a pivotal role in regulating gene expression in development, in response to cellular stress or in disease states, in virtually all cell types. MicroRNAs (miRNAs) are short, non-coding RNA molecules that mediate RNA silencing and regulate gene expression. miRNAs were discovered in 1993 and have been extensively studied ever since. They can be expressed in a tissue-specific manner and play a crucial role in tissue development and many biological processes. miRNAs are responsible for changes in the cell epigenome because of their ability to modulate gene expression post-transcriptionally. Recently, numerous studies have shown that miRNAs and other epigenetic factors can regulate each other or cooperate in regulating several biological processes. On the one hand, the expression of some miRNAs is silenced by DNA methylation, and histone modifications have been demonstrated to modulate miRNA expression in many cell types or disease states. On the other hand, miRNAs can directly target epigenetic factors, such as DNA methyltransferases or histone deacetylases, thus regulating chromatin structure. Moreover, several studies have reported coordinated actions between miRNAs and other epigenetic mechanisms to reinforce the regulation of gene expression. This paper reviews multiple interactions between miRNAs and epigenetic factors in skeletal muscle development and in response to stimuli or disease.

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“…Polycomb-group (PcG) proteins are multiprotein complexes that increase or decrease relative gene expression, accelerating a class of epigenetic events and adding another layer of regulation to gene expression [4]. Previous studies have demonstrated that various combinations of PcG protein complexes contribute to neoplastic progression.…”

Section: Introductionmentioning

confidence: 99%

CBX7 negatively regulates migration and invasion in glioma via Wnt/β-catenin pathway inactivation

Bao

Liu

et al. 2017

Oncotarget

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CBX7, a member of the Polycomb-group proteins, plays a significant role in normal and cancerous tissues and has been defined as a tumor suppressor in thyroid, breast and pancreatic cancers. However, its function in glioma remains undefined. CBX7 expression is decreased in glioma, especially in higher grade cases, according to data in the CGGA, GSE16001 and TCGA databases. Further experimental evidence has shown that exogenous CBX7 overexpression induced apoptosis and inhibited cell proliferation, colony formation and migration of glioma cells. In this study, we show that the invasive ability of glioma cells was decreased following CBX7 overexpression and CBX7 overexpression was associated with Wnt/β-catenin pathway inhibition, which also decreased downstream expression of ZEB1, a core epithelial-to-mesenchymal transition factor. This reduction in Wnt signaling is controlled by DKK1, a specific Wnt/β-catenin inhibitor. CBX7 enhances DKK1 expression by binding the DKK1 promoter, as shown in Luciferase reporter assays. Our data confirm that CBX7 inhibits EMT and invasion in glioma, which is manifested by influencing the expression of MMP2, MMP9, E-cadherin, N-cadherin and Vimentin in LN229, T98G cells and primary glioma cells (PGC). Furthermore, as a tumor suppressor, CBX7 expression is pivotal to reduce tumor invasion and evaluate prognosis.

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The role of Polycomb in stem cell genome architecture

Cited by 27 publications

References 69 publications

Cohesin-dependent and independent mechanisms support chromosomal contacts between promoters and enhancers

Cohesin-dependent and independent mechanisms support chromosomal contacts between promoters and enhancers

Coordinated Actions of MicroRNAs with other Epigenetic Factors Regulate Skeletal Muscle Development and Adaptation

CBX7 negatively regulates migration and invasion in glioma via Wnt/β-catenin pathway inactivation

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