ArticleNature genetics2016
Coordinate redeployment of PRC1 proteins suppresses tumor formation during Drosophila development.
Article in Nature genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 107 citations in OpenAlex.
- More than SAM: mechanisms of action of the Polycomb group protein polyhomeotic.Nucleus (Austin, Tex.) · 2026Review
- Article
- A tumor-suppressive role of the PRC1 Polycomb epigenetic complex in the maintenance of adult Drosophila intestinal stem cell identity.PLoS genetics · 2026Article
- Embryonic stem cell factors DPPA2/4 amplify active H3K4me3-H2AK119ub chromatin domains in non-small cell lung cancer.Genes & development · 2026Article
- Novel modifiers of oncoprotein-mediated Polycomb inhibition in Drosophila melanogaster.Genetics · 2025Article
- BMI1 regulates human erythroid self-renewal through both gene repression and gene activation.Nature communications · 2025Article
- A disordered linker in the Polycomb protein Polyhomeotic tunes phase separation and oligomerization.Molecular cell · 2025Article
- Investigating oncoprotein-mediated chromatin dysregulation inbioRxiv : the preprint server for biology · 2025Article
- A conserved switch to less catalytically active Polycomb repressive complexes in non-dividing cells.Cell reports · 2025Article
- Epigenetic Regulation in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025Review
- Double-strand breaks in facultative heterochromatin require specific movements and chromatin changes for efficient repair.Nature communications · 2024Article
- Epigenetic inheritance and gene expression regulation in early Drosophila embryos.EMBO reports · 2024Review
- Hyd/UBR5 defines a tumor suppressor pathway that links Polycomb repressive complex to regulated protein degradation in tissue growth control and tumorigenesis.Genes & development · 2024Article
- Sustained inactivation of the Polycomb PRC1 complex induces DNA repair defects and genomic instability in epigenetic tumors.Histochemistry and cell biology · 2024Article
- Article
- Article
- Sustained inactivation of the Polycomb PRC1 complex induces DNA repair defects and genomic instability in epigenetic tumors.Research square · 2024Article
- A Two-Step Mechanism for Creating Stable, Condensed Chromatin with the Polycomb Complex PRC1.Molecules (Basel, Switzerland) · 2024Article
- Article
- Polycomb safeguards imaginal disc specification through control of the Vestigial-Scalloped complex.Development (Cambridge, England) · 2023Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Polycomb group proteins form two main complexes, PRC2 and PRC1, which generally coregulate their target genes. Here we show that PRC1 components act as neoplastic tumor suppressors independently of PRC2 function. By mapping the distribution of PRC1 components and trimethylation of histone H3 at Lys27 (H3K27me3) across the genome, we identify a large set of genes that acquire PRC1 in the absence of H3K27me3 in Drosophila larval tissues. These genes massively outnumber canonical targets and are mainly involved in the regulation of cell proliferation, signaling and polarity. Alterations in PRC1 components specifically deregulate this set of genes, whereas canonical targets are derepressed in both PRC1 and PRC2 mutants. In human embryonic stem cells, PRC1 components colocalize with H3K27me3 as in Drosophila embryos, whereas in differentiated cell types they are selectively recruited to a large set of proliferation and signaling-associated genes that lack H3K27me3, suggesting that the redeployment of PRC1 components during development is evolutionarily conserved.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.