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10.1073/pnas.1518552112

http://scihub22266oqcxt.onion/10.1073/pnas.1518552112
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suck abstract from ncbi


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pmid26499245
      Proc+Natl+Acad+Sci+U+S+A 2015 ; 112 (47 ): E6456-65
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  • Chromatin extrusion explains key features of loop and domain formation in wild-type and engineered genomes #MMPMID26499245
  • Sanborn AL ; Rao SS ; Huang SC ; Durand NC ; Huntley MH ; Jewett AI ; Bochkov ID ; Chinnappan D ; Cutkosky A ; Li J ; Geeting KP ; Gnirke A ; Melnikov A ; McKenna D ; Stamenova EK ; Lander ES ; Aiden EL
  • Proc Natl Acad Sci U S A 2015[Nov]; 112 (47 ): E6456-65 PMID26499245 show ga
  • We recently used in situ Hi-C to create kilobase-resolution 3D maps of mammalian genomes. Here, we combine these maps with new Hi-C, microscopy, and genome-editing experiments to study the physical structure of chromatin fibers, domains, and loops. We find that the observed contact domains are inconsistent with the equilibrium state for an ordinary condensed polymer. Combining Hi-C data and novel mathematical theorems, we show that contact domains are also not consistent with a fractal globule. Instead, we use physical simulations to study two models of genome folding. In one, intermonomer attraction during polymer condensation leads to formation of an anisotropic "tension globule." In the other, CCCTC-binding factor (CTCF) and cohesin act together to extrude unknotted loops during interphase. Both models are consistent with the observed contact domains and with the observation that contact domains tend to form inside loops. However, the extrusion model explains a far wider array of observations, such as why loops tend not to overlap and why the CTCF-binding motifs at pairs of loop anchors lie in the convergent orientation. Finally, we perform 13 genome-editing experiments examining the effect of altering CTCF-binding sites on chromatin folding. The convergent rule correctly predicts the affected loops in every case. Moreover, the extrusion model accurately predicts in silico the 3D maps resulting from each experiment using only the location of CTCF-binding sites in the WT. Thus, we show that it is possible to disrupt, restore, and move loops and domains using targeted mutations as small as a single base pair.
  • |*Genetic Engineering [MESH]
  • |*Nucleic Acid Conformation [MESH]
  • |Anisotropy [MESH]
  • |Base Pairing [MESH]
  • |CCCTC-Binding Factor [MESH]
  • |Cell Cycle Proteins/metabolism [MESH]
  • |Chromatin/*chemistry/*genetics [MESH]
  • |Chromosomal Proteins, Non-Histone/metabolism [MESH]
  • |Cohesins [MESH]
  • |Computer Simulation [MESH]
  • |Diffusion [MESH]
  • |Fractals [MESH]
  • |Genome/*genetics [MESH]
  • |Humans [MESH]
  • |In Situ Hybridization, Fluorescence [MESH]
  • |Models, Molecular [MESH]
  • |Nucleotide Motifs/genetics [MESH]
  • |Polymers/chemistry [MESH]
  • |Probability [MESH]


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