Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hierarchical recruitment of Polycomb complexes revisited.

ABSTRACT: Polycomb Group (PcG) proteins epigenetically repress key developmental genes and thereby control alternative cell fates. PcG proteins act as complexes that can modify histones and these histone modifications play a role in transmitting the "memory" of the repressed state as cells divide. Here we consider mainstream models that link histone modifications to hierarchical recruitment of PcG complexes and compare them to results of a direct test of interdependence between PcG complexes for recruitment to Drosophila genes. The direct test indicates that PcG complexes do not rely on histone modifications to recognize their target genes but use them to stabilize the interactions within large chromatin domains. It also shows that multiple strategies are used to coordinate the targeting of PcG complexes to different genes, which may make the repression of these genes more or less robust.

SUBMITTER: Dorafshan E

PROVIDER: S-EPMC5703234 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Hierarchical recruitment of Polycomb complexes revisited.

Dorafshan Eshagh E Kahn Tatyana G TG Schwartz Yuri B YB

Nucleus (Austin, Tex.) 20170914 5

Polycomb Group (PcG) proteins epigenetically repress key developmental genes and thereby control alternative cell fates. PcG proteins act as complexes that can modify histones and these histone modifications play a role in transmitting the "memory" of the repressed state as cells divide. Here we consider mainstream models that link histone modifications to hierarchical recruitment of PcG complexes and compare them to results of a direct test of interdependence between PcG complexes for recruitme ...[more]

PMID: 28910569

Similar Datasets

REST-mediated recruitment of polycomb repressor complexes in mammalian cells.

Project description:Polycomb Repressive Complex (PRC) 1 and PRC2 regulate genes involved in differentiation and development. However, the mechanism for how PRC1 and PRC2 are recruited to genes in mammalian cells is unclear. Here we present evidence for an interaction between the transcription factor REST, PRC1, and PRC2 and show that RNF2 and REST co-regulate a number of neuronal genes in human teratocarcinoma cells (NT2-D1). Using NT2-D1 cells as a model of neuronal differentiation, we furthermore showed that retinoic-acid stimulation led to displacement of PRC1 at REST binding sites, reduced H3K27Me3, and increased gene expression. Genome-wide analysis of Polycomb binding in Rest?/? and Eed?/? mouse embryonic stem (mES) cells showed that Rest was required for PRC1 recruitment to a subset of Polycomb regulated neuronal genes. Furthermore, we found that PRC1 can be recruited to Rest binding sites independently of CpG islands and the H3K27Me3 mark. Surprisingly, PRC2 was frequently increased around Rest binding sites located in CpG-rich regions in the Rest?/? mES cells, indicating a more complex interplay where Rest also can limit PRC2 recruitment. Therefore, we propose that Rest has context-dependent functions for PRC1- and PRC2- recruitment, which allows this transcription factor to act both as a recruiter of Polycomb as well as a limiting factor for PRC2 recruitment at CpG islands.

| S-EPMC3291536 | biostudies-literature

Proximity-dependent recruitment of Polycomb repressive complexes by the lncRNA Airn.

Project description:During mouse embryogenesis, expression of the long non-coding RNA (lncRNA) Airn leads to gene repression and recruitment of Polycomb repressive complexes (PRCs) to varying extents over a 15-Mb domain. The mechanisms remain unclear. Using high-resolution approaches, we show in mouse trophoblast stem cells that Airn expression induces long-range changes to chromatin architecture that coincide with PRC-directed modifications and center around CpG island promoters that contact the Airn locus even in the absence of Airn expression. Intensity of contact between the Airn lncRNA and chromatin correlated with underlying intensity of PRC recruitment and PRC-directed modifications. Deletion of CpG islands that contact the Airn locus altered long-distance repression and PRC activity in a manner that correlated with changes in chromatin architecture. Our data imply that the extent to which Airn expression recruits PRCs to chromatin is controlled by DNA regulatory elements that modulate proximity of the Airn lncRNA product to its target DNA.

| S-EPMC10441531 | biostudies-literature

REST–Mediated Recruitment of Polycomb Repressor Complexes in Mammalian Cells

Project description:Genome-wide analysis of REST and Polycomb binding in Rest-/- and Eed-/- mouse embryonic stem (mES) cells showed that Rest was required for PRC1 recruitment to a subset of Polycomb regulated neuronal genes. Furthermore, we found that PRC1 can be recruited to Rest binding sites independently of CpG islands and the H3K27Me3 mark., and that PRC2 was frequently increased around Rest binding sites located in CpG-rich regions in the Rest2/2 mES cells. Published here: PLoS Genet 8(3): e1002494. doi:10.1371/journal.pgen.1002494 Examination of REST and Polycomb binding in Rest-/-, Eed-/-, and wt mES cells using ChIP-sequencing. Submitter cannot locate the raw data for GSM1169003, GSM1169004, GSM1169011, GSM1169012, GSM1169015, and GSM1169016.

2013-06-20 | E-GEOD-48122 | biostudies-arrayexpress

REST–Mediated Recruitment of Polycomb Repressor Complexes in Mammalian Cells

2013-06-20 | GSE48122 | GEO

LANA-Mediated Recruitment of Host Polycomb Repressive Complexes onto the KSHV Genome during De Novo Infection.

Project description:One of the hallmarks of the latent phase of Kaposi's sarcoma-associated herpesvirus (KSHV) infection is the global repression of lytic viral gene expression. Following de novo KSHV infection, the establishment of latency involves the chromatinization of the incoming viral genomes and recruitment of the host Polycomb repressive complexes (PRC1 and PRC2) to the promoters of lytic genes, which is accompanied by the inhibition of lytic genes. However, the mechanism of how PRCs are recruited to the KSHV episome is still unknown. Utilizing a genetic screen of latent genes in the context of KSHV genome, we identified the latency-associated nuclear antigen (LANA) to be responsible for the genome-wide recruitment of PRCs onto the lytic promoters following infection. We found that LANA initially bound to the KSHV genome right after infection and subsequently recruited PRCs onto the viral lytic promoters, thereby repressing lytic gene expression. Furthermore, both the DNA and chromatin binding activities of LANA were required for the binding of LANA to the KSHV promoters, which was necessary for the recruitment of PRC2 to the lytic promoters during de novo KSHV infection. Consequently, the LANA-knockout KSHV could not recruit PRCs to its viral genome upon de novo infection, resulting in aberrant lytic gene expression and dysregulation of expression of host genes involved in cell cycle and proliferation pathways. In this report, we demonstrate that KSHV LANA recruits host PRCs onto the lytic promoters to suppress lytic gene expression following de novo infection.

| S-EPMC5015872 | biostudies-literature

Proximity-dependent recruitment of Polycomb Repressive Complexes by the lncRNA Airn

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

2023-07-01 | GSE217262 | GEO

Proximity-dependent recruitment of Polycomb Repressive Complexes by the lncRNA Airn [ChIP-Seq]

Project description:Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) in mouse F1-hybrid trophoblast stem cells for PRC subunits and PRC-induced chromatin modifications.

2023-07-01 | GSE220464 | GEO

Proximity-dependent recruitment of Polycomb Repressive Complexes by the lncRNA Airn [CHART-Seq]

Project description:In the developing mouse embryo, expression of the lncRNA Airn induces gene silencing and recruits Polycomb Repressive Complexes (PRCs) to varying extents over a 15 megabase domain, but the mechanisms remain unclear. Using high-resolution approaches, we show in mouse trophoblast stem cells that Airn expression induces long-range changes to chromatin architecture centered around a network of CpG islands occupied by PRCs and SMC1A/Cohesin. Extent of contact with Airn predicts underlying intensity of Polycomb-directed chromatin modifications and Airn-induced changes to chromatin architecture. Deletion of individual CpG islands alternately increase or decrease gene silencing and PRC activity over the domain in a manner predicted by changes in chromatin architecture. We conclude that Airn is a potent repressive lncRNA whose effects are controlled by an equilibratory network of DNA regulatory elements that modulate its frequency of contact with target chromatin.

2023-07-01 | GSE217261 | GEO

Proximity-dependent recruitment of Polycomb Repressive Complexes by the lncRNA Airn [RNA-Seq]

2023-07-01 | GSE217239 | GEO