Journal
NUCLEUS
Volume 9, Issue 1, Pages 20-32Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/19491034.2017.1389365
Keywords
CTCF; cohesin; 3D genome; single-molecule imaging; dynamics; FRAP; topological domains; chromatin loops; loop extrusion; modeling
Categories
Funding
- National Institutes of Health [UO1-EB021236, U54-DK107980]
- Siebel Stem Cell institute
- California Institute of Regenerative Medicine [LA1-08013]
- Howard Hughes Medical Institute [003061]
- NATIONAL INSTITUTE OF BIOMEDICAL IMAGING AND BIOENGINEERING [U01EB021236] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [U54DK107980] Funding Source: NIH RePORTER
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Mammalian genomes are folded into spatial domains, which regulate gene expression by modulating enhancer-promoter contacts. Here, we review recent studies on the structure and function of Topologically Associating Domains (TADs) and chromatin loops. We discuss how loop extrusion models can explain TAD formation and evidence that TADs are formed by the ring-shaped protein complex, cohesin, and that TAD boundaries are established by the DNA-binding protein, CTCF. We discuss our recent genomic, biochemical and single-molecule imaging studies on CTCF and cohesin, which suggest that TADs and chromatin loops are dynamic structures. We highlight complementary polymer simulation studies and Hi-C studies employing acute depletion of CTCF and cohesin, which also support such a dynamic model. We discuss the limitations of each approach and conclude that in aggregate the available evidence argues against stable loops and supports a model where TADs are dynamic structures that continually form and break throughout the cell cycle.
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