CTCF mediates long-range chromatin looping and local histone modification in the β-globin locus

By Erik Splinter, H. Heath, J. Kooren, Robert-Jan Palstra, P. Klous, F. Grosveld, Niels Galjart, W. de Laat. 2006

226 citations recorded by the source corpus.

CTCF (CCCTC-binding factor) binds sites around the mouse beta-globin locus that spatially cluster in the erythroid cell nucleus. We show that both conditional deletion of CTCF and targeted disruption of a DNA-binding site destabilize these long-range interactions and cause local loss of histone acetylation and gain of histone methylation, apparently without affecting transcription at the locus. Our data demonstrate that CTCF is directly involved in chromatin architecture and regulates local balance between active and repressive chromatin marks. We postulate that throughout the genome, relative position and stability of CTCF-mediated loops determine their effect on enhancer-promoter interactions, with gene insulation as one possible outcome.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/d73e8f0266090a224e7929d7165bbcea2d7788b4

Citations in the corpus

• CRISPR Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function (2015, unknown): “The b-globin gene cluster is located between CBS3 (50HS5) and CBS4 (30HS1) in domain1 (Figure 5A) (Hou et al., 2010; Splinter et al., 2006).”
• Architectural protein subclasses shape 3D organization of genomes during lineage commitment. (2013, unknown): “The top three candidates fulfilling these criteria were CCCTC-binding factor (CTCF), cohesin, and Mediator (Hadjur et al., 2009; Handoko et al., 2011; Kagey et al., 2010; Kurukuti et al., 2006; Splinter et al., 2006).”
• Widespread plasticity in CTCF occupancy linked to DNA methylation (2012, unknown): “…genomic processes, including transcription (Baniahmad et al. 1990; Filippova et al. 1996; Vostrov and Quitschke 1997), imprinting (Bell and Felsenfeld 2000; Hark et al. 2000), and long-range chromatin interactions and subnuclear localization (Yusufzai et al. 2004; Splinter 2006; Hou et al. 2008).”
• Topologically associating domains and chromatin loops depend on cohesin and are regulated by CTCF, WAPL, and PDS5 proteins (2017, unknown): “Because CTCF affects gene expression by chromatin looping (Kurukuti et al, 2006; Splinter et al, 2006), it has been speculated that CTCF and cohesin have discrete functions in chromatin organization, with CTCF specifying the genomic sites at which cohesin functions, and cohesin entrapping DNA…”
• YY1 Is a Structural Regulator of Enhancer-Promoter Loops (2017, unknown): “CTCF proteins bound at enhancers and promoters can interact with one another and may thus facilitate enhancerpromoter interactions (Guo et al., 2015; Splinter et al., 2006), but CTCF does not generally occupy these interacting elements (Cuddapah et al., 2009; Kim et al., 2007; Phillips-Cremins et…”
• CTCF-Mediated Functional Chromatin Interactome in Pluripotent Cells (2011, unknown): “Thus, CTCF-associated DNA looping can facilitate communication between regulatory elements, such as enhancers and promoters, and influence transcription, as previously suggeste”
• CTCF: Master Weaver of the Genome (2009, unknown): “Subsequent ChIP experiments confirmed direct CTCF binding to three sites upstream (5′HS85, 5′HS62/60, and 5′HS5) and one downstream (3′HS1) of the mouse β-globin locus (Bulger et al., 2003; Splinter et al., 2006).”