ArticleG3 (Bethesda, Md.)2013
The Drosophila enhancer of split gene complex: architecture and coordinate regulation by notch, cohesin, and polycomb group proteins.
Article in G3 (Bethesda, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Cornelia de Lange Syndrome as Paradigm of Chromatinopathies.Frontiers in neuroscience · 2021Review
- The Many Roles of Cohesin in Drosophila Gene Transcription.Trends in genetics : TIG · 2019Review
- Article
- Brca2, Pds5 and Wapl differentially control cohesin chromosome association and function.PLoS genetics · 2018Article
- Polycomb repressive complex 1 modifies transcription of active genes.Science advances · 2017Article
- ASXL1 interacts with the cohesin complex to maintain chromatid separation and gene expression for normal hematopoiesis.Science advances · 2017Article
- Interdependence of PRC1 and PRC2 for recruitment to Polycomb Response Elements.Nucleic acids research · 2016Article
- Notch signalling mediates reproductive constraint in the adult worker honeybee.Nature communications · 2016Article
- Article
- Functional Conservation of the Glide/Gcm Regulatory Network Controlling Glia, Hemocyte, and Tendon Cell Differentiation in Drosophila.Genetics · 2016Article
- Origin and evolution of the enhancer of split complex.BMC genomics · 2015Article
- Checks and balances between cohesin and polycomb in gene silencing and transcription.Current biology : CB · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The cohesin protein complex functionally interacts with Polycomb group (PcG) silencing proteins to control expression of several key developmental genes, such as the Drosophila Enhancer of split gene complex [E(spl)-C]. The E(spl)-C contains 12 genes that inhibit neural development. In a cell line derived from the central nervous system, cohesin and the PRC1 PcG protein complex bind and repress E (spl)-C transcription, but the repression mechanisms are unknown. The genes in the E(spl)-C are directly activated by the Notch receptor. Here we show that depletion of cohesin or PRC1 increases binding of the Notch intracellular fragment to genes in the E(spl)-C, correlating with increased transcription. The increased transcription likely reflects both direct effects of cohesin and PRC1 on RNA polymerase activity at the E(spl)-C, and increased expression of Notch ligands. By chromosome conformation capture we find that the E(spl)-C is organized into a self-interactive architectural domain that is co-extensive with the region that binds cohesin and PcG complexes. The self-interactive architecture is formed independently of cohesin or PcG proteins. We posit that the E(spl)-C architecture dictates where cohesin and PcG complexes bind and act when they are recruited by as yet unidentified factors, thereby controlling the E(spl)-C as a coordinated domain.
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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.