The DOI matches its Crossref record; 159 of the 159 references it cites were found in a registry or an index.
Occupying Chromatin: Polycomb Mechanisms for Getting to Genomic Targets, Stopping Transcriptional Traffic, and Staying Put
Open accessAbstract
Summary Polycomb repressive complexes are conserved chromatin regulators with key roles in multicellular development, stem cell biology, and cancer. New findings advance molecular understanding of how they target to sites of action, interact with and alter local chromatin to silence genes, and maintain silencing in successive generations of proliferating cells. Chromatin modification by Polycomb proteins provides an essential strategy for gene silencing in higher eukaryotes. Polycomb repressive complexes (PRCs) silence many key developmental regulators and are centrally integrated in the transcriptional circuitry of embryonic and adult stem cells. PRC2 trimethylates histone H3 on lysine-27 (H3-K27me3) and PRC1-type complexes ubiquitylate histone H2A and compact polynucleosomes. How PRCs and these signature activities are deployed to select and silence genomic targets is the subject of intense current investigation. We review recent advances on targeting, modulation, and functions of PRC1 and PRC2, and we consider progress on defining transcriptional steps impacted in Polycomb silencing. Key recent findings demonstrate PRC1 targeting independent of H3-K27me3 and emphasize nonenzymatic PRC1-mediated compaction. We also evaluate expanding connections between Polycomb machinery and non-coding RNAs. Exciting new studies supply the first systematic analyses of what happens to Polycomb complexes, and associated histone modifications, during the wholesale chromatin reorganizations that accompany DNA replication and mitosis. The stage is now set to reveal fundamental epigenetic mechanisms that determine how Polycomb target genes are silenced and how Polycomb silence is preserved through cell cycle progression.
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Citations
Cites
Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis
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Role of Histone H3 Lysine 27 Methylation in Polycomb-Group Silencing
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Cited by
Epigenetic plasticity and the hallmarks of cancer
Flavahan, W. A., Gaskell, E., & Bernstein, B. E. (2017) · Science · doi:10.1126/science.aal2380 · Cited by 1,340
“Context-specific repression of lineage-specific developmental genes is enforced by Polycomb repressors, such as the histone H3 Lys(27) (H3K27) methyltransferase EZH2 (enhancer of zeste homolog 2) (6, 16).”
BackgroundBender, S., Tang, Y., Lindroth, A. M., Hovestadt, V., Jones, D. T. W., Kool, M., Zapatka, M., Northcott, P. A., Sturm, D., Wang, W., et al. (2013) · Cancer Cell · doi:10.1016/j.ccr.2013.10.006 · Cited by 818
Adaptive Chromatin Remodeling Drives Glioblastoma Stem Cell Plasticity and Drug Tolerance
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Maintaining cell identity: PRC2-mediated regulation of transcription and cancer
Comet, I., Riising, E. M., Leblanc, B., & Helin, K. (2016) · Nature Reviews Cancer · doi:10.1038/nrc.2016.83 · Cited by 432
Polycomb repressive complex PRC1 spatially constrains the mouse embryonic stem cell genome
Schoenfelder, S., Sugar, R., Dimond, A., Javierre, B.-M., Armstrong, H., Mifsud, B., Dimitrova, E., Matheson, L., Tavares-Cadete, F., Furlan-Magaril, M., et al. (2015) · Nature Genetics · doi:10.1038/ng.3393 · Cited by 398
Metadata
- Authors
- Simon, J. A., & Kingston, R. E.
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2013-03
- Volume
- 49
- Issue
- 5
- Pages
- 808-824
- ISSN
- 1097-2765 (ISSN-L)
- OpenAlex
- W2123419812
- Cited by
- 733
- References
- 159
- FWCI
- 41.69
- Type
- journal article
- Language
- en
- Open access
- bronze
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