Journal
CELL
Volume 171, Issue 2, Pages 305-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2017.09.026
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Funding
- Paul and Daisy Soros Fellowship
- Fannie and John Hertz Foundation
- Cornelia de Lange Syndrome Foundation
- Stanford Medical Scholars Fellowship
- NIGMS [R01GM055164]
- NIH [1DP2OD008540-01, U01HL130010]
- NSF Physics Frontier Center Grant (Center for Theoretical Biological Physics) [PHY-1427654]
- NHGRI Center for Excellence for Genomic Sciences [HG006193]
- Welch Foundation [Q-1866]
- NVIDIA Research Center
- IBM University
- Google Research Award
- Cancer Prevention Research Institute of Texas [R1304]
- McNair Medical Institute
- NIH Encyclopedia of DNA Elements Mapping Center [UM1HG009375]
- President's Early Career Award in Science and Engineering [4DP2OD008540]
- Division Of Physics
- Direct For Mathematical & Physical Scien [1427654] Funding Source: National Science Foundation
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The human genome folds to create thousands of intervals, called contactdomains,'' that exhibit enhanced contact frequency within themselves. Loop domains'' form because of tethering between two loci-almost always bound by CTCF and cohesin-lying on the same chromosome. Compartment domains'' form when genomic intervals with similar histone marks co-segregate. Here, we explore the effects of degrading cohesin. All loop domains are eliminated, but neither compartment domains nor histone marks are affected. Loss of loop domains does not lead to widespread ectopic gene activation but does affect a significant minority of active genes. In particular, cohesin loss causes superenhancers to co-localize, forming hundreds of links within and across chromosomes and affecting the regulation of nearby genes. We then restore cohesin and monitor the re-formation of each loop. Although reformation rates vary greatly, many megabase-sized loops recovered in under an hour, consistent with a model where loop extrusion is rapid.
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