Polycomb purification by in vivo biotinylation tagging reveals cohesin and Trithorax group proteins as interaction partners

Strübbe, Gero; Popp, Christian; Schmidt, Alexander; Pauli, Andrea; Ringrose, Leonie; Beisel, Christian; Paro, Renato

doi:10.1073/pnas.1007916108

Cited by 98 publications

(98 citation statements)

References 43 publications

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“…Interestingly, control of Scr also depends on interactions between regulatory elements, most probably PREs (Southworth and Kennison, 2002). These data, combined with data showing a biochemical interaction between cohesin and PcG proteins (Strübbe et al, 2011), suggest that cohesin might directly inhibit PcG function. (Gause et al, 2010) of the FRAP recovery curves.…”

Section: Research Articlementioning

confidence: 82%

Wapl antagonizes cohesin binding and promotes Polycomb-group silencing inDrosophila

et al. 2012

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Wapl protein regulates binding of the cohesin complex to chromosomes during interphase and helps remove cohesin from chromosomes at mitosis. We isolated a dominant mutation in wapl (waplAG) in a screen for mutations that counteract silencing mediated by an engrailed Polycomb-group response element. waplAG hemizygotes die as pharate adults and have an extra sex combs phenotype characteristic of males with mutations in Polycomb-group (PcG) genes. The wapl gene encodes two proteins, a long form and a short form. waplAG introduces a stop codon at amino acid 271 of the long form and produces a truncated protein. The expression of a transgene encoding the truncated Wapl-AG protein causes an extra-sex-comb phenotype similar to that seen in the waplAG mutant. Mutations in the cohesin-associated genes Nipped-B and pds5 suppress and enhance waplAG phenotypes, respectively. A Pds5-Wapl complex (releasin) removes cohesin from DNA, while Nipped-B loads cohesin. This suggests that Wapl-AG might exert its effects through changes in cohesin binding. Consistent with this model, Wapl-AG was found to increase the stability of cohesin binding to polytene chromosomes. Our data suggest that increasing cohesin stability interferes with PcG silencing at genes that are co-regulated by cohesin and PcG proteins.

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Section: Research Articlementioning

confidence: 82%

Wapl antagonizes cohesin binding and promotes Polycomb-group silencing inDrosophila

et al. 2012

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“…It is known that Grh is phosphorylated both in vivo and in vitro, and that the mitogen activated kinase (MAPK) pathway can regulate Grh activity Hemphala et al 2003;Zhai et al 2008;Wang et al 2009;Kim and McGinnis 2011). Grh has also been found to interact with Polycomb and Trithorax group proteins, suggesting that Grh may function to recruit corepressors or coactivators to distinct loci (Tuckfield et al 2002;Blastyak et al 2006;Strubbe et al 2011;Hopkin et al 2012). It will be important to investigate the role of these regulatory mechanisms in controlling Grh activity.…”

Section: Discussionmentioning

confidence: 99%

Stable Binding of the Conserved Transcription Factor Grainy Head to its Target Genes ThroughoutDrosophila melanogasterDevelopment

et al. 2017

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It has been suggested that transcription factor binding is temporally dynamic, and that changes in binding determine transcriptional output. Nonetheless, this model is based on relatively few examples in which transcription factor binding has been assayed at multiple developmental stages. The essential transcription factor Grainy head (Grh) is conserved from fungi to humans, and controls epithelial development and barrier formation in numerous tissues. Drosophila melanogaster, which possess a single grainy head (grh) gene, provide an excellent system to study this conserved factor. To determine whether temporally distinct binding events allow Grh to control cell fate specification in different tissue types, we used a combination of ChIP-seq and RNA-seq to elucidate the gene regulatory network controlled by Grh during four stages of embryonic development (spanning stages 5-17) and in larval tissue. Contrary to expectations, we discovered that Grh remains bound to at least 1146 genomic loci over days of development. In contrast to this stable DNA occupancy, the subset of genes whose expression is regulated by Grh varies. Grh transitions from functioning primarily as a transcriptional repressor early in development to functioning predominantly as an activator later. Our data reveal that Grh binds to target genes well before the Grh-dependent transcriptional program commences, suggesting it sets the stage for subsequent recruitment of additional factors that execute stage-specific Grh functions.

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“…6C). Recent evidence suggests that cohesin, which interacts physically with PRC1 (61), is required for the recruitment of PRC1 to promoters of some active genes, many of which exhibit Pol II pausing (22). Loss of PC or other PRC1 components has been shown to lead to an increase in Pol II on the bodies of these genes, suggesting that PRC1 may influence Pol II pausing and/or elongation (22).…”

Section: Discussionmentioning

confidence: 99%

Polycomb inhibits histone acetylation by CBP by binding directly to its catalytic domain

Tie

Banerjee

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Drosophila Polycomb (PC), a subunit of Polycomb repressive complex 1 (PRC1), is well known for its role in maintaining repression of the homeotic genes and many others and for its binding to trimethylated histone H3 on Lys 27 (H3K27me3) via its chromodomain. Here, we identify a novel activity of PC: inhibition of the histone acetylation activity of CREB-binding protein (CBP). We show that PC and its mammalian CBX orthologs interact directly with the histone acetyltransferase (HAT) domain of CBP, binding to the previously identified autoregulatory loop, whose autoacetylation greatly enhances HAT activity. We identify a conserved PC motif adjacent to the chromodomain required for CBP binding and show that PC binding inhibits acetylation of histone H3. CBP autoacetylation impairs PC binding in vitro, and PC is preferentially associated with unacetylated CBP in vivo. PC knockdown elevates the acetylated H3K27 (H3K27ac) level globally and at promoter regions of some genes that are bound by both PC and CBP. Conversely, PC overexpression decreases the H3K27ac level in vivo and also suppresses CBP-dependent Polycomb phenotypes caused by overexpression of Trithorax, an antagonist of Polycomb silencing. We find that PC is physically associated with the initiating form of RNA polymerase II (Pol II) and that many promoters co-occupied by PC and CBP are associated with paused Pol II, suggesting that PC may play a role in Pol II pausing. These results suggest that PC/PRC1 inhibition of CBP HAT activity plays a role in regulating transcription of both repressed and active PC-regulated genes.Polycomb | CBP | acetylation | histone H3K27 | Drosophila

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Polycomb purification by in vivo biotinylation tagging reveals cohesin and Trithorax group proteins as interaction partners

Cited by 98 publications

References 43 publications

Wapl antagonizes cohesin binding and promotes Polycomb-group silencing inDrosophila

Wapl antagonizes cohesin binding and promotes Polycomb-group silencing inDrosophila

Stable Binding of the Conserved Transcription Factor Grainy Head to its Target Genes ThroughoutDrosophila melanogasterDevelopment

Polycomb inhibits histone acetylation by CBP by binding directly to its catalytic domain

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