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Journal articles on the topic 'Polycomb complex'

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Author: Grafiati

Published: 31 August 2024

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1

Strutt, H., and R. Paro. "The polycomb group protein complex of Drosophila melanogaster has different compositions at different target genes." Molecular and Cellular Biology 17, no. 12 (December 1997): 6773–83. http://dx.doi.org/10.1128/mcb.17.12.6773.

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In Drosophila the Polycomb group genes are required for the long-term maintenance of the repressed state of many developmental regulatory genes. Their gene products are thought to function in a common multimeric complex that associates with Polycomb group response elements (PREs) in target genes and regulates higher-order chromatin structure. We show that the chromodomain of Polycomb is necessary for protein-protein interactions within a Polycomb-Polyhomeotic complex. In addition, Posterior Sex Combs protein coimmunoprecipitates Polycomb and Polyhomeotic, indicating that they are members of a common multimeric protein complex. Immunoprecipitation experiments using in vivo cross-linked chromatin indicate that these three Polycomb group proteins are associated with identical regulatory elements of the selector gene engrailed in tissue culture cells. Polycomb, Polyhomeotic, and Posterior Sex Combs are, however, differentially distributed on regulatory sequences of the engrailed-related gene invected. This suggests that there may be multiple different Polycomb group protein complexes which function at different target sites. Furthermore, Polyhomeotic and Posterior Sex Combs are also associated with expressed genes. Polyhomeotic and Posterior Sex Combs may participate in a more general transcriptional mechanism that causes modulated gene repression, whereas the inclusion of Polycomb protein in the complex at PREs leads to stable silencing.

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2

Chiang, A., M. B. O'Connor, R. Paro, J. Simon, and W. Bender. "Discrete Polycomb-binding sites in each parasegmental domain of the bithorax complex." Development 121, no. 6 (June 1, 1995): 1681–89. http://dx.doi.org/10.1242/dev.121.6.1681.

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The Polycomb protein of Drosophila melanogaster maintains the segmental expression limits of the homeotic genes in the bithorax complex. Polycomb-binding sites within the bithorax complex were mapped by immunostaining of salivary gland polytene chromosomes. Polycomb bound to four DNA fragments, one in each of four successive parasegmental regulatory regions. These fragments correspond exactly to the ones that can maintain segmentally limited expression of a lacZ reporter gene. Thus, Polycomb acts directly on discrete multiple sites in bithorax regulatory DNA. Constructs combining fragments from different regulatory regions demonstrate that Polycomb-dependent maintenance elements can act on multiple pattern initiation elements, and that maintenance elements can work together. The cooperative action of maintenance elements may motivate the linear order of the bithorax complex.

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3

De, Sandip, Natalie D. Gehred, Miki Fujioka, Fountane W. Chan, James B. Jaynes, and Judith A. Kassis. "Defining the Boundaries of Polycomb Domains in Drosophila." Genetics 216, no. 3 (September 18, 2020): 689–700. http://dx.doi.org/10.1534/genetics.120.303642.

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Polycomb group (PcG) proteins are an important group of transcriptional repressors that act by modifying chromatin. PcG target genes are covered by the repressive chromatin mark H3K27me3. Polycomb repressive complex 2 (PRC2) is a multiprotein complex that is responsible for generating H3K27me3. In Drosophila, PRC2 is recruited by Polycomb Response Elements (PREs) and then trimethylates flanking nucleosomes, spreading the H3K27me3 mark over large regions of the genome, the “Polycomb domains.” What defines the boundary of a Polycomb domain? There is experimental evidence that insulators, PolII, and active transcription can all form the boundaries of Polycomb domains. Here we divide the boundaries of larval Polycomb domains into six different categories. In one category, genes are transcribed toward the Polycomb domain, where active transcription is thought to stop the spreading of H3K27me3. In agreement with this, we show that introducing a transcriptional terminator into such a transcription unit causes an extension of the Polycomb domain. Additional data suggest that active transcription of a boundary gene may restrict the range of enhancer activity of a Polycomb-regulated gene.

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4

Seong, Ihn Sik, Juliana M. Woda, Ji-Joon Song, Alejandro Lloret, Priyanka D. Abeyrathne, Caroline J. Woo, Gillian Gregory, et al. "Huntingtin facilitates polycomb repressive complex 2." Human Molecular Genetics 19, no. 4 (November 23, 2009): 573–83. http://dx.doi.org/10.1093/hmg/ddp524.

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5

Mohd-Sarip, Adone, Jan A. van der Knaap, Claire Wyman, Roland Kanaar, Paul Schedl, and C. Peter Verrijzer. "Architecture of a Polycomb Nucleoprotein Complex." Molecular Cell 24, no. 1 (October 2006): 91–100. http://dx.doi.org/10.1016/j.molcel.2006.08.007.

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6

Iwata, Shintaro, Hisanori Takenobu, Hajime Kageyama, Haruhiko Koseki, Takeshi Ishii, Atsuko Nakazawa, Shin-ichiro Tatezaki, Akira Nakagawara, and Takehiko Kamijo. "Polycomb group molecule PHC3 regulates polycomb complex composition and prognosis of osteosarcoma." Cancer Science 101, no. 7 (April 7, 2010): 1646–52. http://dx.doi.org/10.1111/j.1349-7006.2010.01586.x.

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7

Ali, Janann Y., and Welcome Bender. "Cross-Regulation among the Polycomb Group Genes in Drosophila melanogaster." Molecular and Cellular Biology 24, no. 17 (September 1, 2004): 7737–47. http://dx.doi.org/10.1128/mcb.24.17.7737-7747.2004.

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ABSTRACT Genes of the Polycomb group in Drosophila melanogaster function as long-term transcriptional repressors. A few members of the group encode proteins found in two evolutionarily conserved chromatin complexes, Polycomb repressive complex 1 (PRC1) and the ESC-E(Z) complex. The majority of the group, lacking clear biochemical functions, might be indirect regulators. The transcript levels of seven Polycomb group genes were assayed in embryos mutant for various other genes in the family. Three Polycomb group genes were identified as upstream positive regulators of the core components of PRC1. There is also negative feedback regulation of some PRC1 core components by other PRC1 genes. Finally, there is positive regulation of PRC1 components by the ESC-E(Z) complex. These multiple pathways of cross-regulation help to explain the large size of the Polycomb group family of genes, but they complicate the genetic analysis of any single member.

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8

Iragavarapu, Akhil Gargey, Liqi Yao, and Vignesh Kasinath. "Structural insights into the interactions of Polycomb Repressive Complex 2 with chromatin." Biochemical Society Transactions 49, no. 6 (November 8, 2021): 2639–53. http://dx.doi.org/10.1042/bst20210450.

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Polycomb repressive complexes are a family of chromatin modifier enzymes which are critical for regulating gene expression and maintaining cell-type identity. The reversible chemical modifications of histone H3 and H2A by the Polycomb proteins are central to its ability to function as a gene silencer. PRC2 is both a reader and writer of the tri-methylation of histone H3 lysine 27 (H3K27me3) which serves as a marker for transcription repression, and heterochromatin boundaries. Over the last few years, several studies have provided key insights into the mechanisms regulating the recruitment and activation of PRC2 at Polycomb target genes. In this review, we highlight the recent structural studies which have elucidated the roles played by Polycomb cofactor proteins in mediating crosstalk between histone post-translational modifications and the recruitment of PRC2 and the stimulation of PRC2 methyltransferase activity.

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9

Lo, Stanley M., Nitin K. Ahuja, and Nicole J. Francis. "Polycomb Group Protein Suppressor 2 of Zeste Is a Functional Homolog of Posterior Sex Combs." Molecular and Cellular Biology 29, no. 2 (November 3, 2008): 515–25. http://dx.doi.org/10.1128/mcb.01044-08.

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ABSTRACT The Drosophila melanogaster Polycomb group protein Posterior Sex Combs is a component of Polycomb repressive complex 1 and is central to Polycomb group-mediated silencing. A related Polycomb group gene, Suppressor 2 of zeste, is thought to be partially redundant in function. The two proteins share a small region of homology but also contain regions of unconserved sequences. Here we report a biochemical characterization of Suppressor 2 of zeste. Like Posterior Sex Combs, Suppressor 2 of zeste binds DNA, compacts chromatin, and inhibits chromatin remodeling. Interestingly, the regions of the two proteins responsible for these activities lack sequence homology. Suppressor 2 of zeste can also replace Posterior Sex Combs in a functional complex with other Polycomb group proteins, but unlike with their biochemical activities, complex formation is mediated by the region of Suppressor 2 of zeste that is homologous to that of Posterior Sex Combs. Our results establish Suppressor 2 of zeste as a functional homolog of Posterior Sex Combs and suggest that the two proteins operate via similar molecular mechanisms.

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10

LaJeunesse, D., and A. Shearn. "E(z): a polycomb group gene or a trithorax group gene?" Development 122, no. 7 (July 1, 1996): 2189–97. http://dx.doi.org/10.1242/dev.122.7.2189.

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The products of the Polycomb group of genes are cooperatively involved in repressing expression of homeotic selector genes outside of their appropriate anterior/posterior boundaries. Loss of maternal and/or zygotic function of Polycomb group genes results in the ectopic expression of both Antennapedia Complex and Bithorax Complex genes. The products of the trithorax group of genes are cooperatively involved in maintaining active expression of homeotic selector genes within their appropriate anterior/posterior boundaries. Loss of maternal and/or zygotic function of trithorax group genes results in reduced expression of both Antennapedia Complex and Bithorax Complex genes. Although Enhancer of zeste has been classified as a member of the Polycomb group, in this paper we show that Enhancer of zeste can also be classified as a member of the trithorax group. The requirement for Enhancer of zeste activity as either a trithorax group or Polycomb group gene depends on the homeotic selector gene locus as well as on spatial and temporal cues.

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11

Lewis, Zachary A. "Polycomb Group Systems in Fungi: New Models for Understanding Polycomb Repressive Complex 2." Trends in Genetics 33, no. 3 (March 2017): 220–31. http://dx.doi.org/10.1016/j.tig.2017.01.006.

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12

Hu, Chi-Kuo, Wei Wang, Julie Brind’Amour, Param Priya Singh, G. Adam Reeves, Matthew C. Lorincz, Alejandro Sánchez Alvarado, and Anne Brunet. "Vertebrate diapause preserves organisms long term through Polycomb complex members." Science 367, no. 6480 (February 20, 2020): 870–74. http://dx.doi.org/10.1126/science.aaw2601.

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Diapause is a state of suspended development that helps organisms survive extreme environments. How diapause protects living organisms is largely unknown. Using the African turquoise killifish (Nothobranchius furzeri), we show that diapause preserves complex organisms for extremely long periods of time without trade-offs for subsequent adult growth, fertility, and life span. Transcriptome analyses indicate that diapause is an active state, with dynamic regulation of metabolism and organ development genes. The most up-regulated genes in diapause include Polycomb complex members. The chromatin mark regulated by Polycomb, H3K27me3, is maintained at key developmental genes in diapause, and the Polycomb member CBX7 mediates repression of metabolism and muscle genes in diapause. CBX7 is functionally required for muscle preservation and diapause maintenance. Thus, vertebrate diapause is a state of suspended life that is actively maintained by specific chromatin regulators, and this has implications for long-term organism preservation.

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13

Torigata, Kosuke, Okuzaki Daisuke, Satomi Mukai, Akira Hatanaka, Fumiharu Ohka, Daisuke Motooka, Shota Nakamura, et al. "LATS2 Positively Regulates Polycomb Repressive Complex 2." PLOS ONE 11, no. 7 (July 19, 2016): e0158562. http://dx.doi.org/10.1371/journal.pone.0158562.

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14

Barrero, Maria J., and Juan Carlos Izpisua Belmonte. "Polycomb complex recruitment in pluripotent stem cells." Nature Cell Biology 15, no. 4 (April 2013): 348–50. http://dx.doi.org/10.1038/ncb2723.

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15

Rank, Gerhard, Matthias Prestel, and Renato Paro. "Transcription through Intergenic Chromosomal Memory Elements of the Drosophila Bithorax Complex Correlates with an Epigenetic Switch." Molecular and Cellular Biology 22, no. 22 (November 15, 2002): 8026–34. http://dx.doi.org/10.1128/mcb.22.22.8026-8034.2002.

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ABSTRACT The proteins of the trithorax and Polycomb groups maintain the differential expression pattern of homeotic genes established by the early embryonic patterning system during development. These proteins generate stable and heritable chromatin structures by acting via particular chromosomal memory elements. We established a transgenic assay system showing that the Polycomb group response elements bxd and Mcp confer epigenetic inheritance throughout development. With previously published data for the Fab7 cellular memory module, we confirmed the cellular memory function of Polycomb group response elements. In Drosophila melanogaster, several of these memory elements are located in the large intergenic regulatory regions of the homeotic bithorax complex. Using a transgene assay, we showed that transcription through a memory element correlated with the relief of silencing imposed by the Polycomb group proteins and established an epigenetically heritable active chromatin mode. A memory element remodeled by the process of transcription was able to maintain active expression of a reporter gene throughout development. Thus, transcription appears to reset and change epigenetic marks at chromosomal memory elements regulated by the Polycomb and trithorax proteins. Interestingly, in the bithorax complex of D. melanogaster, the segment-specific expression of noncoding intergenic transcripts during embryogenesis seems to fulfill this switching role for memory elements regulating the homeotic genes.

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16

Amiad Pavlov, Daria, CP Unnikannan, Dana Lorber, Gaurav Bajpai, Tsviya Olender, Elizabeth Stoops, Adriana Reuveny, Samuel Safran, and Talila Volk. "The LINC Complex Inhibits Excessive Chromatin Repression." Cells 12, no. 6 (March 18, 2023): 932. http://dx.doi.org/10.3390/cells12060932.

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The Linker of Nucleoskeleton and Cytoskeleton (LINC) complex transduces nuclear mechanical inputs suggested to control chromatin organization and gene expression; however, the underlying mechanism is currently unclear. We show here that the LINC complex is needed to minimize chromatin repression in muscle tissue, where the nuclei are exposed to significant mechanical inputs during muscle contraction. To this end, the genomic binding profiles of Polycomb, Heterochromatin Protein1 (HP1a) repressors, and of RNA-Pol II were studied in Drosophila larval muscles lacking functional LINC complex. A significant increase in the binding of Polycomb and parallel reduction of RNA-Pol-II binding to a set of muscle genes was observed. Consistently, enhanced tri-methylated H3K9 and H3K27 repressive modifications and reduced chromatin activation by H3K9 acetylation were found. Furthermore, larger tri-methylated H3K27me3 repressive clusters, and chromatin redistribution from the nuclear periphery towards nuclear center, were detected in live LINC mutant larval muscles. Computer simulation indicated that the observed dissociation of the chromatin from the nuclear envelope promotes growth of tri-methylated H3K27 repressive clusters. Thus, we suggest that by promoting chromatin–nuclear envelope binding, the LINC complex restricts the size of repressive H3K27 tri-methylated clusters, thereby limiting the binding of Polycomb transcription repressor, directing robust transcription in muscle fibers.

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17

Deckard, Charles E., and Jonathan T. Sczepanski. "Polycomb repressive complex 2 binds RNA irrespective of stereochemistry." Chemical Communications 54, no. 85 (2018): 12061–64. http://dx.doi.org/10.1039/c8cc07433j.

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18

Gahan, James M., Fabian Rentzsch, and Christine E. Schnitzler. "The genetic basis for PRC1 complex diversity emerged early in animal evolution." Proceedings of the National Academy of Sciences 117, no. 37 (August 31, 2020): 22880–89. http://dx.doi.org/10.1073/pnas.2005136117.

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Polycomb group proteins are essential regulators of developmental processes across animals. Despite their importance, studies on Polycomb are often restricted to classical model systems and, as such, little is known about the evolution of these important chromatin regulators. Here we focus on Polycomb Repressive Complex 1 (PRC1) and trace the evolution of core components of canonical and non-canonical PRC1 complexes in animals. Previous work suggested that a major expansion in the number of PRC1 complexes occurred in the vertebrate lineage. We show that the expansion of the Polycomb Group RING Finger (PCGF) protein family, an essential step for the establishment of the large diversity of PRC1 complexes found in vertebrates, predates the bilaterian–cnidarian ancestor. This means that the genetic repertoire necessary to form all major vertebrate PRC1 complexes emerged early in animal evolution, over 550 million years ago. We further show that PCGF5, a gene conserved in cnidarians and vertebrates but lost in all other studied groups, is expressed in the nervous system in the sea anemone Nematostella vectensis, similar to its mammalian counterpart. Together this work provides a framework for understanding the evolution of PRC1 complex diversity and it establishes Nematostella as a promising model system in which the functional ramifications of this diversification can be further explored.

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19

Costa, Silvia, and Caroline Dean. "Storing memories: the distinct phases of Polycomb-mediated silencing of Arabidopsis FLC." Biochemical Society Transactions 47, no. 4 (July 5, 2019): 1187–96. http://dx.doi.org/10.1042/bst20190255.

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Abstract Polycomb-mediated epigenetic silencing is central to correct growth and development in higher eukaryotes. The evolutionarily conserved Polycomb repressive complex 2 (PRC2) transcriptionally silences target genes through a mechanism requiring the histone modification H3K27me3. However, we still do not fully understand what defines Polycomb targets, how their expression state is switched from epigenetically ON to OFF and how silencing is subsequently maintained through many cell divisions. An excellent system in which to dissect the sequence of events underlying an epigenetic switch is the Arabidopsis FLC locus. Exposure to cold temperatures progressively induces a PRC2-dependent switch in an increasing proportion of cells, through a mechanism that is driven by the local chromatin environment. Temporally distinct phases of this silencing mechanism have been identified. First, the locus is transcriptionally silenced in a process involving cold-induced antisense transcripts; second, nucleation at the first exon/intron boundary of a Polycomb complex containing cold-induced accessory proteins induces a metastable epigenetically silenced state; third, a Polycomb complex with a distinct composition spreads across the locus in a process requiring DNA replication to deliver long-term epigenetic silencing. Detailed understanding from this system is likely to provide mechanistic insights important for epigenetic silencing in eukaryotes generally.

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20

Muller, J., S. Gaunt, and P. A. Lawrence. "Function of the Polycomb protein is conserved in mice and flies." Development 121, no. 9 (September 1, 1995): 2847–52. http://dx.doi.org/10.1242/dev.121.9.2847.

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A key aspect of determination--the acquisition and propagation of cell fates--is the initiation of patterns of selector gene expression and their maintenance in groups of cells as they divide and develop. In Drosophila, in those groups of cells where particular selector genes must remain inactive, it is the Polycomb-Group of genes that keep them silenced. Here we show that M33, a mouse homologue of the Drosophila Polycomb protein, can substitute for Polycomb in transgenic flies. Polycomb protein is thought to join with other Polycomb-Group proteins to build a complex that silences selector genes. Since members of this group of proteins have their homologues in mice, our results suggest that the molecular mechanism of cell determination is widely conserved.

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21

Verrijzer, C. Peter. "Goldilocks meets Polycomb." Genes & Development 36, no. 19-20 (October 1, 2022): 1043–45. http://dx.doi.org/10.1101/gad.350248.122.

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The Polycomb system modulates chromatin structure to maintain gene repression during cell differentiation. Polycomb repression involves methylation of histone H3K27 (H3K27me3) by Polycomb repressive complex 2 (PRC2), monoubiquitylation of H2A (H2Aub1) by noncanonical PRC1 (ncPRC1), and chromatin compaction by canonical PRC1 (cPRC1), which is independent of its enzymatic activity. Puzzlingly, Polycomb repression also requires deubiquitylation of H2Aub1 by Polycomb repressive deubiquitinase (PR-DUB). In this issue ofGenes & Development, Bonnet and colleagues (pp. 1046–1061) resolve this paradox by showing that high levels of H2Aub1 inDrosophilalacking PR-DUB activity promotes open chromatin and gene expression in spite of normal H3K27me3 levels and PRC binding. Pertinently, gene repression is restored by concomitant loss of PRC1 E3 ubiquitin ligase activity but depends on its chromatin compaction activity. These findings suggest that PR-DUB ensures just-right levels of H2Aub1 to allow chromatin compaction by cPRC1.

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22

Semprich, Claudia I., Lindsay Davidson, Adriana Amorim Torres, Harshil Patel, James Briscoe, Vicki Metzis, and Kate G. Storey. "ERK1/2 signalling dynamics promote neural differentiation by regulating chromatin accessibility and the polycomb repressive complex." PLOS Biology 20, no. 12 (December 1, 2022): e3000221. http://dx.doi.org/10.1371/journal.pbio.3000221.

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Fibroblast growth factor (FGF) is a neural inducer in many vertebrate embryos, but how it regulates chromatin organization to coordinate the activation of neural genes is unclear. Moreover, for differentiation to progress, FGF signalling must decline. Why these signalling dynamics are required has not been determined. Here, we show that dephosphorylation of the FGF effector kinase ERK1/2 rapidly increases chromatin accessibility at neural genes in mouse embryos, and, using ATAC-seq in human embryonic stem cell derived spinal cord precursors, we demonstrate that this occurs genome-wide across neural genes. Importantly, ERK1/2 inhibition induces precocious neural gene transcription, and this involves dissociation of the polycomb repressive complex from key gene loci. This takes place independently of subsequent loss of the repressive histone mark H3K27me3 and transcriptional onset. Transient ERK1/2 inhibition is sufficient for the dissociation of the repressive complex, and this is not reversed on resumption of ERK1/2 signalling. Moreover, genomic footprinting of sites identified by ATAC-seq together with ChIP-seq for polycomb protein Ring1B revealed that ERK1/2 inhibition promotes the occupancy of neural transcription factors (TFs) at non-polycomb as well as polycomb associated sites. Together, these findings indicate that ERK1/2 signalling decline promotes global changes in chromatin accessibility and TF binding at neural genes by directing polycomb and other regulators and appears to serve as a gating mechanism that provides directionality to the process of differentiation.

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23

Chen, Xin, Mark Hiller, Yasemin Sancak, and Margaret T. Fuller. "Tissue-Specific TAFs Counteract Polycomb to Turn on Terminal Differentiation." Science 310, no. 5749 (November 3, 2005): 869–72. http://dx.doi.org/10.1126/science.1118101.

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Polycomb transcriptional silencing machinery is implicated in the maintenance of precursor fates, but how this repression is reversed to allow cell differentiation is unknown. Here we show that testis-specific TAF (TBP-associated factor) homologs required for terminal differentiation of male germ cells may activate target gene expression in part by counteracting repression by Polycomb. Chromatin immunoprecipitation revealed that testis TAFs bind to target promoters, reduce Polycomb binding, and promote local accumulation of H3K4me3, a mark of Trithorax action. Testis TAFs also promoted relocalization of Polycomb Repression Complex 1 components to the nucleolus in spermatocytes, implicating subnuclear architecture in the regulation of terminal differentiation.

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24

Fitzgerald, Daniel P., and Welcome Bender. "Polycomb Group Repression Reduces DNA Accessibility." Molecular and Cellular Biology 21, no. 19 (October 1, 2001): 6585–97. http://dx.doi.org/10.1128/mcb.21.19.6585-6597.2001.

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ABSTRACT The Polycomb group proteins are responsible for long-term repression of a number of genes in Drosophila melanogaster, including the homeotic genes of the bithorax complex. The Polycomb protein is thought to alter the chromatin structure of its target genes, but there has been little direct evidence for this model. In this study, the chromatin structure of the bithorax complex was probed with three separate assays for DNA accessibility: (i) activation of polymerase II (Pol II) transcription by Gal4, (ii) transcription by the bacteriophage T7 RNA polymerase (T7RNAP), and (iii) FLP-mediated site-specific recombination. All three processes are restricted or blocked in Polycomb-repressed segments. In contrast, control test sites outside of the bithorax complex permitted Gal4, T7RNAP, and FLP activities throughout the embryo. Several P insertions in the bithorax complex were tested, providing evidence that thePolycomb-induced effect is widespread over target genes. This accessibility effect is similar to that seen for SIR silencing inSaccharomyces cerevisiae. In contrast to SIR silencing, however, episomes excised fromPolycomb-repressed chromosomal sites do not show an altered superhelix density.

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25

AN, Yan-Rong, Jian-Bin XU, and Hai-Long AN. "Polycomb group protein complex involved in plant vernalization." Hereditas (Beijing) 33, no. 3 (May 6, 2011): 207–12. http://dx.doi.org/10.3724/sp.j.1005.2011.00207.

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26

Davidovich, Chen, Leon Zheng, Karen J. Goodrich, and Thomas R. Cech. "Promiscuous RNA binding by Polycomb repressive complex 2." Nature Structural & Molecular Biology 20, no. 11 (September 29, 2013): 1250–57. http://dx.doi.org/10.1038/nsmb.2679.

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27

Francis, N. J. "Chromatin Compaction by a Polycomb Group Protein Complex." Science 306, no. 5701 (November 26, 2004): 1574–77. http://dx.doi.org/10.1126/science.1100576.

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28

Francis, Nicole J., Andrew J. Saurin, Zhaohui Shao, and Robert E. Kingston. "Reconstitution of a Functional Core Polycomb Repressive Complex." Molecular Cell 8, no. 3 (September 2001): 545–56. http://dx.doi.org/10.1016/s1097-2765(01)00316-1.

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29

Bratkowski, Matthew, Xin Yang, and Xin Liu. "Polycomb repressive complex 2 in an autoinhibited state." Journal of Biological Chemistry 292, no. 32 (June 12, 2017): 13323–32. http://dx.doi.org/10.1074/jbc.m117.787572.

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30

Danishuddin, Naidu Subbarao, Mohammad Faheem, and Shahper Nazeer Khan. "Polycomb repressive complex 2 inhibitors: emerging epigenetic modulators." Drug Discovery Today 24, no. 1 (January 2019): 179–88. http://dx.doi.org/10.1016/j.drudis.2018.07.002.

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31

Kouznetsova, Valentina L., Alex Tchekanov, Xiaoming Li, Xiaowen Yan, and Igor F. Tsigelny. "Polycomb repressive 2 complex—Molecular mechanisms of function." Protein Science 28, no. 8 (June 10, 2019): 1387–99. http://dx.doi.org/10.1002/pro.3647.

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32

Naxerova, Kamila. "A new function for polycomb in immune evasion." Science Translational Medicine 11, no. 514 (October 16, 2019): eaaz3718. http://dx.doi.org/10.1126/scitranslmed.aaz3718.

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33

Kanhere, Aditi, Keijo Viiri, Carla C. Araújo, Jane Rasaiyaah, Russell D. Bouwman, Warren A. Whyte, C. Filipe Pereira, et al. "Short RNAs Are Transcribed from Repressed Polycomb Target Genes and Interact with Polycomb Repressive Complex-2." Molecular Cell 38, no. 5 (June 2010): 675–88. http://dx.doi.org/10.1016/j.molcel.2010.03.019.

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34

Flora, Pooja, Gil Dalal, Idan Cohen, and Elena Ezhkova. "Polycomb Repressive Complex(es) and Their Role in Adult Stem Cells." Genes 12, no. 10 (September 24, 2021): 1485. http://dx.doi.org/10.3390/genes12101485.

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Populations of resident stem cells (SCs) are responsible for maintaining, repairing, and regenerating adult tissues. In addition to having the capacity to generate all the differentiated cell types of the tissue, adult SCs undergo long periods of quiescence within the niche to maintain themselves. The process of SC renewal and differentiation is tightly regulated for proper tissue regeneration throughout an organisms’ lifetime. Epigenetic regulators, such as the polycomb group (PcG) of proteins have been implicated in modulating gene expression in adult SCs to maintain homeostatic and regenerative balances in adult tissues. In this review, we summarize the recent findings that elucidate the composition and function of the polycomb repressive complex machinery and highlight their role in diverse adult stem cell compartments.

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35

Vijayanathan, Mallika, María Guadalupe Trejo-Arellano, and Iva Mozgová. "Polycomb Repressive Complex 2 in Eukaryotes—An Evolutionary Perspective." Epigenomes 6, no. 1 (January 17, 2022): 3. http://dx.doi.org/10.3390/epigenomes6010003.

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Polycomb repressive complex 2 (PRC2) represents a group of evolutionarily conserved multi-subunit complexes that repress gene transcription by introducing trimethylation of lysine 27 on histone 3 (H3K27me3). PRC2 activity is of key importance for cell identity specification and developmental phase transitions in animals and plants. The composition, biochemistry, and developmental function of PRC2 in animal and flowering plant model species are relatively well described. Recent evidence demonstrates the presence of PRC2 complexes in various eukaryotic supergroups, suggesting conservation of the complex and its function. Here, we provide an overview of the current understanding of PRC2-mediated repression in different representatives of eukaryotic supergroups with a focus on the green lineage. By comparison of PRC2 in different eukaryotes, we highlight the possible common and diverged features suggesting evolutionary implications and outline emerging questions and directions for future research of polycomb repression and its evolution.

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Veneti, Zoe, Kalliopi Gkouskou, and Aristides Eliopoulos. "Polycomb Repressor Complex 2 in Genomic Instability and Cancer." International Journal of Molecular Sciences 18, no. 8 (July 30, 2017): 1657. http://dx.doi.org/10.3390/ijms18081657.

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Benoit, Y. D., M. B. Lepage, T. Khalfaoui, E. Tremblay, N. Basora, J. C. Carrier, L. J. Gudas, and J. F. Beaulieu. "Polycomb repressive complex 2 impedes intestinal cell terminal differentiation." Journal of Cell Science 125, no. 14 (March 30, 2012): 3454–63. http://dx.doi.org/10.1242/jcs.102061.

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Margueron, Raphaël, and Danny Reinberg. "The Polycomb complex PRC2 and its mark in life." Nature 469, no. 7330 (January 2011): 343–49. http://dx.doi.org/10.1038/nature09784.

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Shao, Zhaohui, Florian Raible, Ramin Mollaaghababa, Jeffrey R. Guyon, Chao-ting Wu, Welcome Bender, and Robert E. Kingston. "Stabilization of Chromatin Structure by PRC1, a Polycomb Complex." Cell 98, no. 1 (July 1999): 37–46. http://dx.doi.org/10.1016/s0092-8674(00)80604-2.

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Cifuentes-Rojas, Catherine, Alfredo J. Hernandez, Kavitha Sarma, and Jeannie T. Lee. "Regulatory Interactions between RNA and Polycomb Repressive Complex 2." Molecular Cell 55, no. 2 (July 2014): 171–85. http://dx.doi.org/10.1016/j.molcel.2014.05.009.

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Zhang, Jisheng, Evan Bardot, and Elena Ezhkova. "Epigenetic regulation of skin: focus on the Polycomb complex." Cellular and Molecular Life Sciences 69, no. 13 (February 7, 2012): 2161–72. http://dx.doi.org/10.1007/s00018-012-0920-x.

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Pherson, Michelle, Ziva Misulovin, Maria Gause, Kathie Mihindukulasuriya, Amanda Swain, and Dale Dorsett. "Polycomb repressive complex 1 modifies transcription of active genes." Science Advances 3, no. 8 (August 2017): e1700944. http://dx.doi.org/10.1126/sciadv.1700944.

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Lee, Stanley C. W., Belinda Phipson, Craig D. Hyland, Huei San Leong, Rhys S. Allan, Aaron Lun, Douglas J. Hilton, et al. "Polycomb repressive complex 2 (PRC2) suppresses Eμ-myc lymphoma." Blood 122, no. 15 (October 10, 2013): 2654–63. http://dx.doi.org/10.1182/blood-2013-02-484055.

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Moritz, Lindsay E., and Raymond C. Trievel. "Structure, mechanism, and regulation of polycomb-repressive complex 2." Journal of Biological Chemistry 293, no. 36 (September 14, 2017): 13805–14. http://dx.doi.org/10.1074/jbc.r117.800367.

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Molitor, Anne, and Wen-Hui Shen. "The Polycomb Complex PRC1: Composition and Function in Plants." Journal of Genetics and Genomics 40, no. 5 (May 2013): 231–38. http://dx.doi.org/10.1016/j.jgg.2012.12.005.

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Blastyák, András, Rakesh K. Mishra, Francois Karch, and Henrik Gyurkovics. "Efficient and Specific Targeting of Polycomb Group Proteins Requires Cooperative Interaction between Grainyhead and Pleiohomeotic." Molecular and Cellular Biology 26, no. 4 (February 15, 2006): 1434–44. http://dx.doi.org/10.1128/mcb.26.4.1434-1444.2006.

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ABSTRACT Specific targeting of the protein complexes formed by the Polycomb group of proteins is critically required to maintain the inactive state of a group of developmentally regulated genes. Although the role of DNA binding proteins in this process has been well established, it is still not understood how these proteins target the Polycomb complexes specifically to their response elements. Here we show that the grainyhead gene, which encodes a DNA binding protein, interacts with one such Polycomb response element of the bithorax complex. Grainyhead binds to this element in vitro. Moreover, grainyhead interacts genetically with pleiohomeotic in a transgene-based, pairing-dependent silencing assay. Grainyhead also interacts with Pleiohomeotic in vitro, which facilitates the binding of both proteins to their respective target DNAs. Such interactions between two DNA binding proteins could provide the basis for the cooperative assembly of a nucleoprotein complex formed in vitro. Based on these results and the available data, we propose that the role of DNA binding proteins in Polycomb group-dependent silencing could be described by a model very similar to that of an enhanceosome, wherein the unique arrangement of protein-protein interaction modules exposed by the cooperatively interacting DNA binding proteins provides targeting specificity.

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Bakhshinyan, David, Ashley A. Adile, Chitra Venugopal, and Sheila K. Singh. "Bmi1 – A Path to Targeting Cancer Stem Cells." European Oncology & Haematology 13, no. 02 (2017): 147. http://dx.doi.org/10.17925/eoh.2017.13.02.147.

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The Polycomb group (PcG) genes encode for proteins comprising two multiprotein complexes, Polycomb repressive complex 1 (PRC1) and Polycomb repressive complex 2 (PRC2). Although the initial discovery of PcG genes was made in Drosophila, as transcriptional repressors of homeotic (HOX) genes. Polycomb repressive complexes have been since implicated in regulating a wide range of cellular processes, including differentiation and self-renewal in normal and cancer stem cells. Bmi1, a subunit of PRC1, has been long implicated in driving self-renewal, the key property of stem cells. Subsequent studies showing upregulation of Bmi1 in several cancers correlated with increased aggressiveness, radioresistance and metastatic potential, provided rationale for development of targeted therapies against Bmi1. Although Bmi1 activity can be reduced through transcriptional, post-transcriptional and post-translational regulation, to date, the most promising approach has been through small molecule inhibitors targeting Bmi1 activity. The post-translational targeting of Bmi1 in colorectal carcinoma, lung adenocarcinoma, multiple myeloma and medulloblastoma have led to significant reduction of self-renewal capacity of cancer stem cells, leading to slower tumour progression and reduced extent of metastatic spread. Further value of Bmi1 targeting in cancer can be established through trials evaluating the combinatorial effect of Bmi1 inhibition with current ‘gold standard’ therapies.

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Ngubo, Mzwanele, Fereshteh Moradi, Caryn Y. Ito, and William L. Stanford. "Tissue-Specific Tumour Suppressor and Oncogenic Activities of the Polycomb-like Protein MTF2." Genes 14, no. 10 (September 27, 2023): 1879. http://dx.doi.org/10.3390/genes14101879.

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The Polycomb repressive complex 2 (PRC2) is a conserved chromatin-remodelling complex that catalyses the trimethylation of histone H3 lysine 27 (H3K27me3), a mark associated with gene silencing. PRC2 regulates chromatin structure and gene expression during organismal and tissue development and tissue homeostasis in the adult. PRC2 core subunits are associated with various accessory proteins that modulate its function and recruitment to target genes. The multimeric composition of accessory proteins results in two distinct variant complexes of PRC2, PRC2.1 and PRC2.2. Metal response element-binding transcription factor 2 (MTF2) is one of the Polycomb-like proteins (PCLs) that forms the PRC2.1 complex. MTF2 is highly conserved, and as an accessory subunit of PRC2, it has important roles in embryonic stem cell self-renewal and differentiation, development, and cancer progression. Here, we review the impact of MTF2 in PRC2 complex assembly, catalytic activity, and spatiotemporal function. The emerging paradoxical evidence suggesting that MTF2 has divergent roles as either a tumour suppressor or an oncogene in different tissues merits further investigations. Altogether, our review illuminates the context-dependent roles of MTF2 in Polycomb group (PcG) protein-mediated epigenetic regulation. Its impact on disease paves the way for a deeper understanding of epigenetic regulation and novel therapeutic strategies.

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Tang, Bo, Rui Sun, Dejie Wang, Haoyue Sheng, Ting Wei, Liguo Wang, Jun Zhang, et al. "ZMYND8 preferentially binds phosphorylated EZH2 to promote a PRC2-dependent to -independent function switch in hypoxia-inducible factor–activated cancer." Proceedings of the National Academy of Sciences 118, no. 8 (February 16, 2021): e2019052118. http://dx.doi.org/10.1073/pnas.2019052118.

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Both gene repressor (Polycomb-dependent) and activator (Polycomb-independent) functions of the Polycomb protein enhancer of zeste homolog 2 (EZH2) are implicated in cancer progression. EZH2 protein can be phosphorylated at various residues, such as threonine 487 (T487), by CDK1 kinase, and such phosphorylation acts as a Polycomb repressive complex 2 (PRC2) suppression “code” to mediate the gene repressor-to-activator switch of EZH2 functions. Here we demonstrate that the histone reader protein ZMYND8 is overexpressed in human clear cell renal cell carcinoma (ccRCC). ZMYND8 binds to EZH2, and their interaction is largely enhanced by CDK1 phosphorylation of EZH2 at T487. ZMYND8 depletion not only enhances Polycomb-dependent function of EZH2 in hypoxia-exposed breast cancer cells or von Hippel–Lindau (VHL)-deficient ccRCC cells, but also suppresses the FOXM1 transcription program. We further show that ZMYND8 is required for EZH2–FOXM1 interaction and is important for FOXM1-dependent matrix metalloproteinase (MMP) gene expression and EZH2-mediated migration and invasion of VHL-deficient ccRCC cells. Our results identify a previously uncharacterized role of the chromatin reader ZMYND8 in recognizing the PRC2-inhibitory phosphorylation “code” essential for the Polycomb-dependent to -independent switch of EZH2 functions. They also reveal an oncogenic pathway driving cell migration and invasion in hypoxia-inducible factor–activated (hypoxia or VHL-deficient) cancer.

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Faucheux, M., J. Y. Roignant, S. Netter, J. Charollais, C. Antoniewski, and L. Théodore. "batman Interacts with Polycomb and trithorax Group Genes and Encodes a BTB/POZ Protein That Is Included in a Complex Containing GAGA Factor." Molecular and Cellular Biology 23, no. 4 (February 15, 2003): 1181–95. http://dx.doi.org/10.1128/mcb.23.4.1181-1195.2003.

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ABSTRACT Polycomb and trithorax group genes maintain the appropriate repressed or activated state of homeotic gene expression throughout Drosophila melanogaster development. We have previously identified the batman gene as a Polycomb group candidate since its function is necessary for the repression of Sex combs reduced. However, our present genetic analysis indicates functions of batman in both activation and repression of homeotic genes. The 127-amino-acid Batman protein is almost reduced to a BTB/POZ domain, an evolutionary conserved protein-protein interaction domain found in a large protein family. We show that this domain is involved in the interaction between Batman and the DNA binding GAGA factor encoded by the Trithorax-like gene. The GAGA factor and Batman codistribute on polytene chromosomes, coimmunoprecipitate from nuclear embryonic and larval extracts, and interact in the yeast two-hybrid assay. Batman, together with the GAGA factor, binds to MHS-70, a 70-bp fragment of the bithoraxoid Polycomb response element. This binding, like that of the GAGA factor, requires the presence of d(GA)n sequences. Together, our results suggest that batman belongs to a subset of the Polycomb/trithorax group of genes that includes Trithorax-like, whose products are involved in both activation and repression of homeotic genes.

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