Polycomb and bmi-1 homologs are expressed in overlapping patterns in Xenopus embryos and are able to interact with each other

Reijnen, Marlene J.; Hamer, Karien M.; Blaauwen, Jan L. den; Lambrechts, Caro; Schoneveld, Ilse; Driel, Roel van; Otte, Arie P.

doi:10.1016/0925-4773(95)00422-x

Cited by 50 publications

(54 citation statements)

References 39 publications

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“…To isolate human Pc homologs, we screened a human fetal brain cDNA library with a probe that encompasses the coding region of a Xenopus Pc homolog, XPc, except for the chromodomain (33). We isolated an 1,867-bp cDNA clone ( Fig.…”

Section: Resultsmentioning

confidence: 99%

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Interference with the Expression of a Novel Human Polycomb Protein, hPc2, Results in Cellular Transformation and Apoptosis

Satijn

Olson

Vlag

et al. 1997

Molecular and Cellular Biology

108

123

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Polycomb (Pc) is involved in the stable and heritable repression of homeotic gene activity during Drosophila development. Here, we report the identification of a novel human Pc homolog, hPc2. This gene is more closely related to a Xenopus Pc homolog, XPc, than to a previously described human Pc homolog, CBX2 (hPc1). However, the hPc2 and CBX2/hPc1 proteins colocalize in interphase nuclei of human U-2 OS osteosarcoma cells, suggesting that the proteins are part of a common protein complex. To study the functions of the novel human Pc homolog, we generated a mutant protein, ⌬hPc2, which lacks an evolutionarily conserved C-terminal domain. This C-terminal domain is important for hPc2 function, since the ⌬hPc2 mutant protein which lacks the C-terminal domain is unable to repress gene activity. Expression of the ⌬hPc2 protein, but not of the wild-type hPc2 protein, results in cellular transformation of mammalian cell lines as judged by phenotypic changes, altered marker gene expression, and anchorage-independent growth. Specifically in ⌬hPc2-transformed cells, the expression of the c-myc proto-oncogene is strongly enhanced and serum deprivation results in apoptosis. In contrast, overexpression of the wild-type hPc2 protein results in decreased c-myc expression. Our data suggest that hPc2 is a repressor of proto-oncogene activity and that interference with hPc2 function can lead to derepression of proto-oncogene transcription and subsequently to cellular transformation.

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Section: Resultsmentioning

confidence: 99%

“…Several vertebrate homologs of Pc have been identified (15,30,33), suggesting that repression of gene activity, mediated by Pc, is evolutionarily conserved. This idea is supported by the finding that a mouse Pc homolog, M33, is able to rescue the Drosophila Pc phenotype (25).…”

mentioning

confidence: 99%

Interference with the Expression of a Novel Human Polycomb Protein, hPc2, Results in Cellular Transformation and Apoptosis

Satijn

Olson

Vlag

et al. 1997

Molecular and Cellular Biology

108

123

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“…Expression profiles of both PRC1 and PRC2 components ( Fig. 1 and data not shown; see also Reijnen et al, 1995;Aldiri and Vetter, 2009) reveal that PcG transcripts are located primarily in the neural and the neural crest cells during Xenopus neurulation, suggesting that they regulate development of these tissues. Consistent with this notion, we show here that PRC2 modulates expression of late, but not early, neural markers and controls neural crest development.…”

Section: Discussionmentioning

confidence: 99%

Snail2/Slug cooperates with Polycomb repressive complex 2 (PRC2) to regulate neural crest development

et al. 2015

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Neural crest cells arise from the border of the neural plate and epidermal ectoderm, migrate extensively and differentiate into diverse cell types during vertebrate embryogenesis. Although much has been learnt about growth factor signals and gene regulatory networks that regulate neural crest development, limited information is available on how epigenetic mechanisms control this process. In this study, we show that Polycomb repressive complex 2 (PRC2) cooperates with the transcription factor Snail2/Slug to modulate neural crest development in Xenopus. The PRC2 core components Eed, Ezh2 and Suz12 are expressed in the neural crest cells and are required for neural crest marker expression. Knockdown of Ezh2, the catalytic subunit of PRC2 for histone H3K27 methylation, results in defects in neural crest specification, migration and craniofacial cartilage formation. EZH2 interacts directly with Snail2, and Snail2 fails to expand the neural crest domains in the absence of Ezh2. Chromatin immunoprecipitation analysis shows that Snail2 regulates EZH2 occupancy and histone H3K27 trimethylation levels at the promoter region of the Snail2 target E-cadherin. Our results indicate that Snail2 cooperates with EZH2 and PRC2 to control expression of the genes important for neural crest specification and migration during neural crest development.

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“…However, the identification of the polycomb group (Pc-G) of repressors from Drosophila, and the functionally homologous yeast Rme1p [144], Xenopus XPc [145] and human HPH1 [146,147] proteins has revealed a mechanism which overcomes this requirement [148].…”

Section: Polycomb Group Proteinsmentioning

confidence: 99%

Transcriptional control and the role of silencers in transcriptional regulation in eukaryotes

Ogbourne

Antalis

1998

Biochemical Journal

225

171

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Mechanisms controlling transcription and its regulation are fundamental to our understanding of molecular biology and, ultimately, cellular biology. Our knowledge of transcription initiation and integral factors such as RNA polymerase is considerable, and more recently our understanding of the involvement of enhancers and complexes such as holoenzyme and mediator has increased dramatically. However, an understanding of transcriptional repression is also essential for a complete understanding of promoter structure and the regulation of gene expression. Transcriptional repression in eukaryotes is achieved through ‘silencers ’, of which there are two types, namely ‘silencer elements ’ and ‘negative regulatory elements ’ (NREs). Silencer elements are classical, position-independent elements that direct an active repression mechanism, and NREs are position-dependent elements that direct a passive repression mechanism. In addition, ‘repressors ’ are DNA-binding trasncription factors that interact directly with silencers. A review of the recent literature reveals that it is the silencer itself and its context within a given promoter, rather than the interacting repressor, that determines the mechanism of repression. Silencers form an intrinsic part of many eukaryotic promoters and, consequently, knowledge of their interactive role with enchancers and other transcriptional elements is essential for our understanding of gene regulation in eukaryotes.

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Polycomb and bmi-1 homologs are expressed in overlapping patterns in Xenopus embryos and are able to interact with each other

Cited by 50 publications

References 39 publications

Interference with the Expression of a Novel Human Polycomb Protein, hPc2, Results in Cellular Transformation and Apoptosis

Interference with the Expression of a Novel Human Polycomb Protein, hPc2, Results in Cellular Transformation and Apoptosis

Snail2/Slug cooperates with Polycomb repressive complex 2 (PRC2) to regulate neural crest development

Transcriptional control and the role of silencers in transcriptional regulation in eukaryotes

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