text:
ibroblasts,G1 Phase,Resting Phase; Cell Cycle},
  pages = {1239-1249},
  file = {/home/bbeltr1/Documents/paper-collection/TraskB/Yokota et al_1995_Evidence for the organization of chromatin in megabase pair-sized loops.pdf},
  pmid = {7559748},
  pmcid = {PMC2120584}
}

@article{brower-toland2002,
  title = {Mechanical Disruption of Individual Nucleosomes Reveals a Reversible Multistage Release of {{DNA}}},
  volume = {99},
  copyright = {Copyright \textcopyright{} 2002, The National Academy of Sciences},
  issn = {0027-8424, 1091-6490},
  abstract = {The dynamic structure of individual nucleosomes was examined by stretching nucleosomal arrays with a feedback-enhanced optical trap. Forced disassembly of each nucleosome occurred in three stages. Analysis of the data using a simple worm-like chain model yields 76 bp of DNA released from the histone core at low stretching force. Subsequently, 80 bp are released at higher forces in two stages: full extension of DNA with histones bound, followed by detachment of histones. When arrays were relaxed before the dissociated state was reached, nucleosomes were able to reassemble and to repeat the disassembly process. The kinetic parameters for nucleosome disassembly also have been determined.},
  language = {en},
  number = {4},
  journal = {PNAS},
  doi = {10.1073/pnas.022638399},
  author = {{Brower-Toland}, Brent D. and Smith, Corey L. and Yeh, Richard C. and Lis, John T. and Peterson, Craig L. and Wang, Michelle D.},
  month = feb,
  year = {2002},
  pages = {1960-1965},
  file = {/home/bbeltr1/Documents/paper-collection/WangM/Brower-Toland et al_2002_Mechanical disruption of individual nucleosomes reveals a reversible multistage.pdf;/home/bbeltr1/Documents/zotero/storage/8E5SZHAI/1960.html},
  pmid = {11854495}
}

@incollection{langowski2006,
  title = {Chromatin {{Simulations}}},
  isbn = {978-1-4020-4794-7},
  language = {en},
  booktitle = {Computational {{Studies}} of {{RNA}} and {{DNA}}},
  publisher = {{Springer Netherlands}},
  author = {Langowski, J. and Schiessel, H.},
  editor = {{\v S}poner, J. and Lanka{\v s}, F.},
  year = {2006},
  pages = {605-634},
  file = {/home/bbeltr1/Documents/paper-collection/SchiesselH/Langowski_Schiessel_2006_Chromatin Simulations.pdf},
  doi = {10.1007/978-1-4020-4851-3_24}
}

@article{wedemann2002,
  title = {Computer {{Simulation}} of the 30-{{Nanometer Chromatin Fiber}}},
  volume = {82},
  issn = {0006-3495},
  abstract = {A new Monte Carlo model for the structure of chromatin is presented here. Based on our previous work on superhelical DNA and polynucleosomes, it reintegrates aspects of the ``solenoid'' and the ``zig-zag'' models. The DNA is modeled as a flexible elastic polymer chain, consisting of segments connected by elastic bending, torsional, and stretching springs. The electrostatic interaction between the DNA segments is described by the Debye-H\"uckel approximation. Nucleosome core particles are represented by oblate ellipsoids; their interaction potential has been parameterized by a comparison with data from liquid crystals of nucleosome solutions. DNA and chromatosomes are linked either at the surface of the chromatosome or through a rigid nucleosome stem. Equilibrium ensembles of 100-nucleosome chains at physiological ionic strength were generated by a Metropolis-Monte Carlo algorithm. For a DNA linked at the nucleosome stem and a nucleosome repeat of 200 bp, the simulated fiber diameter of 32nm and the mass density of 6.1 nucleosomes per 11nm fiber length are in excellent agreement with experimental values from the literature. The experimental value of the inclination of DNA and nucleosomes to the fiber axis could also be reproduced. Whereas the linker DNA connects chromatosomes on opposite sides of the fiber, the overall packing of the nucleosomes leads to a helical aspect of the structure. The persistence length of the simulated fibers is 265nm. For more random fibers where the tilt angles between two nucleosomes are chosen according to a Gaussian distribution along the fiber, the persistence length decreases to 30nm with increasing width of the distribution, whereas the other observable parameters such as the mass density remain unchanged. Polynucleosomes with repeat lengths of 212 bp also form fibers with the expected experimental properties. Systems with larger repeat length form fibers, but the mass density is significantly lower than the measured value. The theoretical characteristics of a fiber with a repeat length of 192 bp where DNA and nucleosomes are connected at the core particle are in agreement with the experimental values. Systems without a stem and a repeat length of 217 bp do not form fibers.},
  number = {6},
  journal = {Biophysical Journal},
  doi = {10.1016/S0006-3495(02)75627-0},
  author = {Wedemann, Gero and Langowski, J\"org},
  month = jun,
  year = {2002},
  pages = {2847-2859},
  file = {/home/bbeltr1/Documents/paper-collection/LangowskiJ/Wedemann_Langowski_2002_Computer Simulation of the 30-Nanometer Chromatin Fiber.pdf;/home/bbeltr1/Documents/zotero/storage/JLMHGB5H/S0006349502756270.html}
}

@article{wocjan2009,
  title = {Brownian Dynamics Simulation of {{DNA}} Unrolling from the Nucleosome},
  volume = {113},
  issn = {1520-6106},
  abstract = {Nucleosomes organize chromatin in eukaryotic cells at the lowest scale by wrapping the DNA double helix around a histone octamer. The mechanism by which this structure can be opened, giving access to DNA-processing enzymes, is of fundamental biological importance. Here we describe a new coarse-grained model based on the toroidal geometry of the nucleosome which allows the simulation of nucleosome stretching experiments with a Brownian dynamics algorithm including hydrodynamics. We obtain force-extension curves and calculate energy barriers and kinetic rate constants of the unrolling transition from rupture forces.},
  language = {eng},
  number = {9},
  journal = {J Phys Chem B},
  author = {Wocjan, T. and Klenin, K. and Langowski, J.},
  month = mar,
  year = {2009},
  keywords = {Biophysics,Algorithms,Computer Simulation,Kinetics,Polymers,Chromosomes,Nucleosomes,Models; Statistical,DNA,Models; Molecular,Nucleic Acid Conformation,Models; Chemical},
  pages = {2639-2646},
  pmid = {19708203}
}

@article{krajewski1996,
  title = {Modulation of the Higher-Order Folding of Chromatin by Deletion of Histone {{H3}} and {{H4}} Terminal Domains.},
  volume = {316},
  issn = {0264-6021},
  abstract = {The 'tails' of histones H3 and H4 were removed by light in situ trypsin digestion of the nuclei. The alterations in the higher-order folding of chromatin resulting from this treatment were monitored by ethidium bromide titration. We found that DNA-intercalation of ethidium bromide under these conditions exhibited a complex concentration effect that was dependent on the extent of chromatin folding. This most likely reflects the structural transitions of chromatin during its folding as a result of the changes in the nucleosome linker twist [Woodcock, Grigoryev, Horowitz and Whitaker (1993) Proc. Natl. Acad. Sci. U.S.A. 90, 9021-9025]. These results strongly suggest that the H3 and H4 terminal domains play a very important role in chromatin folding. We discuss the molecular basis of this phenomenon and propose a novel generalized model for the higher-order folding of chromatin.},
  number = {Pt 2},
  journal = {Biochem J},
  author = {Krajewski, W A and Ausi\'o, J},
  month = jun,
  year = {1996},
  pages = {395-400},
  file = {/home/bbeltr1/Documents/paper-collection/AusióJ/Krajewski_Ausió_1996_Modulation of the higher-order folding of chromatin by deletion of histone H3.pdf},
  pmid = {8687379},
  pmcid = {PMC1217363}
}

@article{routh2008,
  title = {Nucleosome Repeat Length and Linker Histone Stoichiometry Determine Chromatin Fiber Structure},
  volume = {105},
  issn = {1091-6490},
  abstract = {To understand how nuclear processes involving DNA are regulated, knowledge of the determinants of chromatin condensation is required. From recent structural studies it has been concluded that the formation of the 30-nm chromatin fiber does not require the linker histone. Here, by comparing the linker histone-dependent compaction of long, reconstituted nucleosome arrays with different nucleosome repeat lengths (NRLs), 167 and 197 bp, we establish that the compaction behavior is both NRL- and linker histone-dependent. Only the 197-bp NRL array can form 30-nm higher-order chromatin structure. Importantly for understanding the regulation of compaction, this array shows a cooperative linker histone-dependent compaction. The 167-bp NRL array displays a limited linker histone-dependent compaction, resulting in a thinner and topologically different fiber. These observations provide an explanation for the distribution of NRLs found in nature.},
  language = {eng},
  number = {26},
  journal = {Proc. Natl. Acad. Sci. U.S.A.},
  doi = {10.1073/pnas.0802336105},
  author = {Routh, Andrew and Sandin, Sara and Rhodes, Daniela},
  month = jul,
  year = {2008},
  keywords = {Animals,Histones,Nucleosomes,Protein Binding,Chickens,Base Pairing,Repetitive Sequences; Nucleic Acid},
  pages = {8872-8877},
  pmid = {18583476},
  pmcid = {PMC2440727}
}

@article{correll2012,
  title = {Short Nucleosome Repeats Impose Rotational Modulations on Chromatin Fibre Folding},
  volume = {31},
  copyright = {Copyright \textcopyright{} 2012 European Molecular Biology Organization},
  issn = {1460-2075},
  abstract = {In eukaryotic cells, DNA is organized into arrays of repeated nucleosomes where the shorter nucleosome repeat length (NRL) types are associated with transcriptionally active chromatin. Here, we tested a hypothesis that systematic variations in the NRL influence nucleosome array folding into higher-order structures. For NRLs with fixed rotational settings, we observed a negative correlation between NRL and chromatin folding. Rotational variations within a range of longer NRLs (188 bp and above) typical of repressed chromatin in differentiated cells did not reveal any changes in chromatin folding. In sharp contrast, for the shorter NRL range of 165\textendash{}177 bp, we observed a strong periodic dependence of chromatin folding upon the changes in linker DNA lengths, with the 172 bp repeat found in highly transcribed yeast chromatin imposing an unfolded state of the chromatin fibre that could be reversed by linker histone. Our results suggest that the NRL may direct chromatin higher-order structure into either a nucleosome position-dependent folding for short NRLs typical of transcribed genes or an architectural factor-dependent folding typical of longer NRLs prevailing in eukaryotic heterochromatin.},
  language = {en},
  number = {10},
  journal = {The EMBO Journal},
  doi = {10.1038/emboj.2012.80},
  author = {Correll, Sarah J. and Schubert, Michaela H. and Grigoryev, Sergei A.},
  month = mar,
  year = {2012},
  keywords = {nucleosome,chromatin fibre,higher-order structure,linker DNA,linker histone},
  pages = {2416-2426},
  file = {/home/bbeltr1/Documents/paper-collection/GrigoryevS/Correll et al_2012_Short nucleosome repeats impose rotational modulations on chromatin fibre.pdf;/home/bbeltr1/Documents/zotero/storage/AJME674K/emboj.2012.html}
}

@article{nikitina2017,
  title = {{{DNA}} Topology in Chromatin Is Defined by Nucleosome Spacing},
  volume = {3},
  issn = {2375-2548},
  abstract = {Nucleosome spacing variations cause topological polymorphism of chromatin that can affect DNA supercoiling and transcription., In eukaryotic nucleosomes, DNA makes \textasciitilde{}1.7 superhelical turns around histone octamer. However, there is a long-standing discrepancy between the nucleosome core structure determined by x-ray crystallography and measurements of DNA topology in circular minichromosomes, indicating that there is only \textasciitilde{}1.0 superhelical turn per nucleosome. Although several theoretical assumptions were put forward to explain this paradox by conformational variability of the nucleosome linker, none was tested experimentally. We analyzed topological properties of DNA in circular nucleosome arrays with precisely positioned nucleosomes. Using topological electrophoretic assays and electron microscopy, we demonstrate that the DNA linking number per nucleosome strongly depends on the nucleosome spacing and varies from -1.4 to -0.9. For the predominant \{10n + 5\} class of nucleosome repeats found in native chromatin, our results are consistent with the DNA topology observed earlier. Thus, we reconcile the topological properties of nucleosome arrays with nucleosome core structure and provide a simple explanation for the DNA topology in native chromatin with variable DNA linker length. Topological polymorphism of the chromatin fibers described here may reflect a more general tendency of chromosomal domains containing active or repressed genes to acquire different nucleosome spacing to retain topologically distinct higher-order structures.},
  number = {10},
  journal = {Sci Adv},
  doi = {10.1126/sciadv.1700957},
  author = {Nikitina, Tatiana and Norouzi, Davood and Grigoryev, Sergei A. and Zhurkin, Victor B.},
  month = oct,
  year = {2017},
  file = {/home/bbeltr1/Documents/paper-collection/ZhurkinV/Nikitina et al_2017_DNA topology in chromatin is defined by nucleosome spacing.pdf},
  pmid = {29098179},
  pmcid = {PMC5659657}
}

@article{ris1970,
  title = {Chromosome {{Structure}}},
  volume = {4},
  number = {1},
  journal = {Annual Review of Genetics},
  doi = {10.1146/annurev.ge.04.120170.001403},
  author = {Ris, H and Kubai, D F},
  year = {1970},
  pages = {263-294},
  file = {/home/bbeltr1/Documents/paper-collection/KubaiD/Ris_Kubai_1970_Chromosome Structure.pdf},
  pmid = {4950239}
}

@article{worcel1981,
  title = {Structure of Chromatin and the Linking Number of {{DNA}}.},
  volume = {78},
  issn = {0027-8424},
  abstract = {Recent observations suggest that the basic supranucleosomal structure of chromatin is a zigzag helical ribbon with a repeat unit made of two nucleosomes connected by a relaxed spacer DNA. A remarkable feature of one particular ribbon is that it solves the apparent paradox between the number of DNA turns per nucleosome and the total linking number of a nucleosome-containing closed circular DNA molecule. We show here that the repeat unit of the proposed structure, which contains two nucleosomes with -1 3/4 DNA turns per nucleosome and one spacer crossover per repeat, contributes -2 to the linking number of closed circular DNA. Space-filling models show that the cylindrical 250-A chromatin fiber can be generated by twisting the ribbon.},
  number = {3},
  journal = {Proc Natl Acad Sci U S A},
  author = {Worcel, A and Strogatz, S and Riley, D},
  month = mar,
  year = {1981},
  pages = {1461-1465},
  file = {/home/bbeltr1/Documents/paper-collection/RileyD/Worcel et al_1981_Structure of chromatin and the linking number of DNA.pdf},
  pmid = {6940168},
  pmcid = {PMC319150}
}

@article{williams1986,
  title = {Chromatin Fibers Are Left-Handed Double Helices with Diameter and Mass per Unit Length That Depend on Linker Length},
  volume = {49},
  issn = {0006-3495},
  abstract = {Four classes of models have been proposed for the internal structure of eukaryotic chromosome fibers--the solenoid, twisted-ribbon, crossed-linker, and superbead models. We have collected electron image and x-ray scattering data from nuclei, and isolated chromatin fibers of seven different tissues to distinguish between these models. The fiber diameters are related to the linker lengths by the equation: D(N) = 19.3 + 0.23 N, where D(N) is the external diameter (nm) and N is the linker length (base pairs). The number of nucleosomes per unit length of the fibers is also related to linker length. Detailed studies were done on the highly regular chromatin from erythrocytes of Necturus (mud puppy) and sperm of Thyone (sea cucumber). Necturus chromatin fibers (N = 48 bp) have diameters of 31 nm and have 7.5 +/- 1 nucleosomes per 10 nm along the axis. Thyone chromatin fibers (N = 87 bp) have diameters of 39 nm and have 12 +/- 2 nucleosomes per 10 nm along the axis. Fourier transforms of electron micrographs of Necturus fibers showed left-handed helical symmetry with a pitch of 25.8 +/- 0.8 nm and pitch angle of 32 +/- 3 degrees, consistent with a double helix. Comparable conclusions were drawn from the Thyone data. The data do not support the solenoid, twisted-ribbon, or supranucleosomal particle models. The data do support two crossed-linker models having left-handed double-helical symmetry and conserved nucleosome interactions.},
  number = {1},
  journal = {Biophysical Journal},
  doi = {10.1016/S0006-3495(86)83637-2},
  author = {Williams, S. P. and Athey, B. D. and Muglia, L. J. and Schappe, R. S. and Gough, A. H. and Langmore, J. P.},
  month = jan,
  year = {1986},
  pages = {233-248},
  file = {/home/bbeltr1/Documents/paper-collection/LangmoreJ/Williams et al_1986_Chromatin fibers are left-handed double helices with diameter and mass per unit.pdf;/home/bbeltr1/Documents/zotero/storage/NR5DIPWV/S0006349586836372.html}
}

@article{stolz2010,
  title = {{{ICM Web}}: The Interactive Chromatin Modeling Web Server},
  volume = {38},
  issn = {0305-1048},
  shorttitle = {{{ICM Web}}},
  abstract = {Abstract.  The interactive chromatin modeling web server (ICM Web) is an interactive tool that allows users to rapidly assess nucleosome stability and fold sequ},
  language = {en},
  number = {suppl\_2},
  journal = {Nucleic Acids Res},
  doi = {10.1093/nar/gkq496},
  author = {Stolz, Richard C. and Bishop, Thomas C.},
  month = jul,
  year = {2010},
  pages = {W254-W261},
  file = {/home/bbeltr1/Documents/paper-collection/BishopT/Stolz_Bishop_2010_ICM Web.pdf;/home/bbeltr1/Documents/zotero/storage/R576TXA9/1121181.html}
}

@article{norouzi2015,
  title = {Topological {{Polymorphism}} of the {{Two}}-{{Start Chromatin Fiber}}},
  volume = {108},
  issn = {0006-3495},
  abstract = {Specific details concerning the spatial organization of nucleosomes in 30~nm fibers remain unknown. To investigate this, we analyzed all stereochemically possible configurations of two-start nucleosome fibers with short DNA linkers L~= 13\textendash{}37~bp (nucleosome repeat length (NRL)~= 160\textendash{}184~bp). Four superhelical parameters\textemdash{}inclination of nucleosomes, twist, rise, and diameter\textemdash{}uniquely describe a regular symmetric fiber. The energy of a fiber is defined as the sum of four terms: elastic energy of the linker DNA, steric repulsion, electrostatics, and a phenomenological (H4 tail\textendash{}acidic patch) interaction between two stacked nucleosomes. By optimizing the fiber energy with respect to the superhelical parameters, we found two types of topological transition in fibers (associated with the change in inclination angle): one caused by an abrupt 360\textdegree{} change in the linker DNA twisting (change in the DNA linking number, {$\Delta$}Lk~= 1), and another caused by overcrossing of the linkers ({$\Delta$}Lk~=~2). To the best of our knowledge, this topological polymorphism of the two-start fibers was not reported in the computations published earlier. Importantly, the optimal configurations of the fibers with linkers L~= 10n and 10n~+ 5~bp are characterized by different values of the DNA linking number\textemdash{}that is, they are topologically different. Our results are consistent with experimental observations, such as the inclination 60\textdegree{} to 70\textdegree{} (the angle between the nucleosomal disks and the fiber axis), helical rise, diameter, and left-handedness of the fibers. In addition, we make several testable predictions, among them different degrees of DNA supercoiling in fibers with L~= 10n and 10n~+ 5~bp, different flexibility of the two types of fibers, and a correlation between the local NRL and the level of transcription in different parts of the yeast genome.},
  number = {10},
  journal = {Biophys J},
  doi = {10.1016/j.bpj.2015.04.015},
  author = {Norouzi, Davood and Zhurkin, Victor B.},
  month = may,
  year = {2015},
  pages = {2591-2600},
  file = {/home/bbeltr1/Documents/paper-collection/ZhurkinV/Norouzi_Zhurkin_2015_Topological Polymorphism of the Two-Start Chromatin Fiber.pdf},
  pmid = {25992737},
  pmcid = {PMC4457244}
}

@article{prunell1998,
  title = {A {{Topological Approach}} to {{Nucleosome Structure}} and {{Dynamics}}: {{The Linking Number Paradox}} and {{Other Issues}}},
  volume = {74},
  issn = {0006-3495},
  shorttitle = {A {{Topological Approach}} to {{Nucleosome Structure}} and {{Dynamics}}},
  language = {English},
  number = {5},
  journal = {Biophysical Journal},
  doi = {10.1016/S0006-3495(98)77961-5},
  author = {Prunell, Ariel},
  month = may,
  year = {1998},
  pages = {2531-2544},
  file = {/home/bbeltr1/Documents/paper-collection/PrunellA/Prunell_1998_A Topological Approach to Nucleosome Structure and Dynamics.pdf;/home/bbeltr1/Documents/zotero/storage/K62YGM5X/S0006-3495(98)77961-5.html},
  pmid = {9591679}
}

@article{scipioni2010,
  title = {Geometrical, Conformational and Topological Restraints in Regular Nucleosome Compaction in Chromatin},
  volume = {148},
  issn = {0301-4622},
  abstract = {The folding of the nucleosome array into a chromatin fiber modulates DNA accessibility and is therefore an important factor for the control of gene expression. The statistical analysis of the nucleosome repeat length in chromatin fibers reveals the presence of a ten-fold periodicity suggesting the existence of orientational constraints of the nucleosome units that provide the geometrical conditions of helical conformations. Recently, the elucidation of the x-ray crystal structure of a nucleosome tetramer array and the interpretation of electron microscopy images of reconstituted nucleosome arrays suggested two different architectures of the chromatin fiber. We approached the problem by integrating the experimental findings with geometrical, conformational and topological restraints, under the hypothesis of the minimum distortion of the nucleosome and linker DNA structures. We show that the excluded volume at linker crossing and the torsional energy limit the possible close packing of the nucleosomes in the chromatin fiber. In particular, the torsional energy of the chromatin fiber appears crucial in determining the kind of nucleosome packing for short nucleosome repeat lengths as in telomeres and yeast chromatin.},
  number = {1},
  journal = {Biophysical Chemistry},
  doi = {10.1016/j.bpc.2010.02.010},
  author = {Scipioni, Anita and Turchetti, Giulia and Morosetti, Stefano and De Santis, Pasquale},
  month = may,
  year = {2010},
  keywords = {Conformational equivalence,Nucleosome packing in chromatin,Topological conditions,Torsional energy of linkers},
  pages = {56-67},
  file = {/home/bbeltr1/Documents/paper-collection/De SantisP/Scipioni et al_2010_Geometrical, conformational and topological restraints in regular nucleosome.pdf;/home/bbeltr1/Documents/zotero/storage/4XHEVBR6/S0301462210000384.html}
}

@Article{ghosh2018,
   Author="Ghosh, S. K.  and Jost, D. ",
   Title="{{H}ow epigenome drives chromatin folding and dynamics, insights from efficient coarse-grained models of chromosomes}",
   Journal="PLoS Comput. Biol.",
   Year="2018",
   Volume="14",
   Number="5",
   Pages="e1006159",
   Month="05"
}

@article{brackley2017,
  title = {Nonequilibrium Chromosome Looping via Molecular Slip Links},
  author = {Brackley, C. A. and Johnson, J. and Michieletto, D. and Morozov, A. N. and Nicodemi, M. and Cook, P. R. and Marenduzzo, D.},
  journal = {Phys. Rev. Lett.},
  volume = {119},
  issue = {13},
  pages = {138101},
  numpages = {5},
  year = {2017},
  month = {Sep},
  publisher = {American Physical Society},
  doi = {10.1103/PhysRevLett.119.138101},
  url = {https://link.aps.org/doi/10.1103/PhysRevLett.119.138101}
}

@article{ben2001,
  title={Chromatin: a tunable spring at work inside chromosomes},
  author={Ben-Ha{\"\i}m, Eli and Lesne, Annick and Victor, Jean-Marc},
  journal={Physical Review E},
  volume={64},
  number={5},
  pages={051921},
  year={2001},
  publisher={APS}
}

@Article{rosa2008,
   Author="Rosa, A.  and Everaers, R. ",
   Title="{{S}tructure and dynamics of interphase chromosomes}",
   Journal="PLoS Comput. Biol.",
   Year="2008",
   Volume="4",
   Number="8",
   Pages="e1000153",
   Month="Aug"
}

@article{michieletto2016,
  title = {Polymer Model with {{Epigenetic Recoloring Reveals}} a {{Pathway}} for the {\emph{de Novo}} {{Establishment}} and {{3D Organization}} of {{Chromatin Domains}}},
  volume = {6},
  issn = {2160-3308},
  language = {en},
  number = {4},
  journal = {Physical Review X},
  doi = {10.1103/PhysRevX.6.041047},
  author = {Michieletto, D. and Orlandini, E. and Marenduzzo, D.},
  month = dec,
  year = {2016},
  file = {/home/bbeltr1/Documents/paper-collection/MarenduzzoD/Michieletto et al_2016_Polymer model with Epigenetic Recoloring Reveals a Pathway for the ide.pdf}
}

@phdthesis{castro1994,
  address = {Eugene},
  title = {Measurement of the Elasticity of Single Chromatin Fibers: The Effect of Histone {{H1}}},
  school = {University of Oregon},
  author = {Castro, C.},
  year = {1994}
}

@article{lohr2007,
  title = {Using {{Atomic Force Microscopy To Study Chromatin Structure}} and {{Nucleosome Remodeling}}},
  volume = {41},
  issn = {1046-2023},
  abstract = {Atomic Force Microscopy (AFM) is a technique that can directly image single molecules in solution and it therefore provides a powerful tool for obtaining unique insights into the basic properties of biological materials and the functional processes in which they are involved. We have used AFM to analyze basic features of nucleosomes in arrays, such as DNA-histone binding strength, cooperativity in template occupation, nucleosome stabilities, nucleosome locations and the effects of acetylation, to compare these features in different types of arrays and to track the response of array nucleosomes to the action of the human Swi-Snf ATP-dependent nucleosome remodeling complex. These experiments required several specific adaptations of basic AFM methods, such as repetitive imaging of the same fields of molecules in liquid, the ability to change the environmental conditions of the sample being imaged and detection of specific types of molecules within compositionally complex samples. Here we describe the techniques that allowed such analyses to be carried out.},
  number = {3},
  journal = {Methods},
  doi = {10.1016/j.ymeth.2006.08.016},
  author = {Lohr, D. and Bash, R. and Wang, H. and Yodh, J. and Lindsay, S.},
  month = mar,
  year = {2007},
  pages = {333-341},
  file = {/home/bbeltr1/Documents/paper-collection/LindsayS/Lohr et al_2007_Using Atomic Force Microscopy To Study Chromatin Structure and Nucleosome.pdf},
  pmid = {17309844},
  pmcid = {PMC1876669}
}

@article{maeshima2010,
  series = {Nucleus and Gene Expression},
  title = {Chromatin Structure: Does the 30-Nm Fibre Exist in Vivo?},
  volume = {22},
  issn = {0955-0674},
  shorttitle = {Chromatin Structure},
  abstract = {A long strand of DNA is wrapped around the core histone and forms a nucleosome. Although the nucleosome has long been assumed to be folded into 30-nm chromatin fibres, their structural details and how such fibres are organised into a nucleus or mitotic chromosome remain unclear. When we observed frozen hydrated (vitrified) human mitotic cells using cryo-electron microscopy, which enables direct high-resolution imaging of the cellular structures in a close-to-native state, we found no higher order structures including 30-nm chromatin fibres in the chromosome. Therefore, we propose that the nucleosome fibres exist in a highly disordered, interdigitated state like a `polymer melt' that undergoes dynamic movement. We postulate that a similar state exists in active interphase nuclei, resulting in several advantages in the transcription and DNA replication processes.},
  number = {3},
  journal = {Current Opinion in Cell Biology},
  doi = {10.1016/j.ceb.2010.03.001},
  author = {Maeshima, Kazuhiro and Hihara, Saera and Eltsov, Mikhail},
  month = jun,
  year = {2010},
  pages = {291-297},
  file = {/home/bbeltr1/Documents/paper-collection/EltsovM/Maeshima et al_2010_Chromatin structure.pdf;/home/bbeltr1/Documents/zotero/storage/DNEVUH8L/S0955067410000256.html}
}

@article{tremethick2007,
  title = {Higher-{{Order Structures}} of {{Chromatin}}: {{The Elusive}} 30 Nm {{Fiber}}},
  volume = {128},
  issn = {0092-8674, 1097-4172},
  shorttitle = {Higher-{{Order Structures}} of {{Chromatin}}},
  abstract = {Despite progress in understanding chromatin function, the structure of the 30 nm chromatin fiber has remained elusive. However, with the recent crystal structure of a short tetranucleosomal array, the 30 nm fiber is beginning to come into view.},
  language = {English},
  number = {4},
  journal = {Cell},
  doi = {10.1016/j.cell.2007.02.008},
  author = {Tremethick, David J.},
  month = feb,
  year = {2007},
  pages = {651-654},
  file = {/home/bbeltr1/Documents/paper-collection/TremethickD/Tremethick_2007_Higher-Order Structures of Chromatin.pdf;/home/bbeltr1/Documents/zotero/storage/DHGPBR2D/S0092-8674(07)00188-2.html},
  pmid = {17320503}
}

@article{langmore1983,
  title = {Low Angle X-Ray Diffraction Studies of Chromatin Structure in Vivo and in Isolated Nuclei and Metaphase Chromosomes},
  volume = {96},
  issn = {0021-9525},
  abstract = {Diffraction of x-rays from living cells, isolated nuclei, and metaphase chromosomes gives rise to several major low angle reflections characteristic of a highly conserved pattern of nucleosome packing within the chromatin fibers. We answer three questions about the x-ray data: Which reflections are characteristic of chromosomes in vivo? How can these reflections be preserved in vitro? What chromosome structures give rise to the reflections? Our consistent observation of diffraction peaks at 11.0, 6.0, 3.8, 2.7 and 2.1 nm from a variety of living cells, isolated nuclei, and metaphase chromosomes establishes these periodicities as characteristic of eukaryotic chromosomes in vivo. In addition, a 30-40- nm peak is observed from all somatic cells that have substantial amounts of condensed chromatin, and a weak 18-nm reflection is observed from nucleated erythrocytes. These observations provide a standard for judging the structural integrity of isolated nuclei, chromosomes, and chromatin, and thus resolve long standing controversy about the ``tru'' nature of chromosome diffraction. All of the reflection seen in vivo can be preserved in vitro provided that the proper ionic conditions are maintained. Our results show clearly that the 30-40-nm maximum is a packing reflection. The packing we observe in vivo is directly correlated to the side-by-side arrangement of 20- 30-nm fibers observed in thin sections of fixed and dehydrated cells and isolated chromosomes. This confirms that such packing is present in living cells and is not merely an artifact of electron microscopy. As expected, the packing reflection is shifted to longer spacings when the fibers are spread apart by reducing the concentration of divalent cations in vitro. Because the 18-, 11.0-, 6.0-, 3.8-, 2.7-, and 2.1-nm reflections are not affected by the decondensation caused by removal of divalent cations, these periodicities must reflect the internal structure of the chromaticn fibers.},
  number = {4},
  journal = {J Cell Biol},
  author = {Langmore, JP and Paulson},
  month = apr,
  year = {1983},
  pages = {1120-1131},
  file = {/home/bbeltr1/Documents/paper-collection/Paulson/Langmore_Paulson_1983_Low angle x-ray diffraction studies of chromatin structure in vivo and in.pdf},
  pmid = {6682117},
  pmcid = {PMC2112310}
}

@article{paulson1983,
  title = {Low Angle X-Ray Diffraction Studies of {{HeLa}} Metaphase Chromosomes: Effects of Histone Phosphorylation and Chromosome Isolation Procedure.},
  volume = {96},
  copyright = {\textcopyright{} 1983 Rockefeller University Press},
  issn = {0021-9525, 1540-8140},
  shorttitle = {Low Angle X-Ray Diffraction Studies of {{HeLa}} Metaphase Chromosomes},
  abstract = {To test whether gross changes in chromatin structure occur during the cell cycle, we compared HeLa mitotic metaphase chromosomes and interphase nuclei by low angle x-ray diffraction. Interphase nuclei and metaphase chromosomes differ only in the 30-40-nm packing reflection, but not in the higher angle part of the x-ray diffraction pattern. Our interpretation of these results is that the transition to metaphase affects only the packing of chromatin fibers and not, to the resolution of our method, the internal structure of nucleosomes or the pattern of nucleosome packing within chromatin fibers. In particular, phosphorylation of histones H1 and H3 at mitosis does not affect chromatin fiber structure, since the same x-ray results are obtained whether or not histone dephosphorylation is prevented by isolating metaphase chromosomes in the presence of 5,5'-dithiobis(2-nitrobenzoate) or low concentrations of p-chloromercuriphenylsulfonate (ClHgPhSO3). We also compared metaphase chromosomes isolated by several different published procedures, and found that the isolation procedure can significantly affect the x-ray diffraction pattern. High concentrations of ClHgPhSO3 can also profoundly affect the pattern.},
  language = {en},
  number = {4},
  journal = {The Journal of Cell Biology},
  doi = {10.1083/jcb.96.4.1132},
  author = {Paulson, J. R. and Langmore, J. P.},
  month = apr,
  year = {1983},
  pages = {1132-1137},
  file = {/home/bbeltr1/Documents/paper-collection/LangmoreJ/Paulson_Langmore_1983_Low angle x-ray diffraction studies of HeLa metaphase chromosomes.pdf;/home/bbeltr1/Documents/zotero/storage/WMET7H2K/1132.html},
  pmid = {6833394}
}

@article{nishino2012,
  title = {Human Mitotic Chromosomes Consist Predominantly of Irregularly Folded Nucleosome Fibres without a 30-nm Chromatin Structure},
  volume = {31},
  copyright = {Copyright \textcopyright{} 2012 European Molecular Biology Organization},
  issn = {0261-4189, 1460-2075},
  abstract = {How a long strand of genomic DNA is compacted into a mitotic chromosome remains one of the basic questions in biology. The nucleosome fibre, in which DNA is wrapped around core histones, has long been assumed to be folded into a 30-nm chromatin fibre and further hierarchical regular structures to form mitotic chromosomes, although the actual existence of these regular structures is controversial. Here, we show that human mitotic HeLa chromosomes are mainly composed of irregularly folded nucleosome fibres rather than 30-nm chromatin fibres. Our comprehensive and quantitative study using cryo-electron microscopy and synchrotron X-ray scattering resolved the long-standing contradictions regarding the existence of 30-nm chromatin structures and detected no regular structure {$>$}11 nm. Our finding suggests that the mitotic chromosome consists of irregularly arranged nucleosome fibres, with a fractal nature, which permits a more dynamic and flexible genome organization than would be allowed by static regular structures.
There is a Have you seen? (April 2012) associated with this Article.},
  language = {en},
  number = {7},
  journal = {The EMBO Journal},
  doi = {10.1038/emboj.2012.35},
  author = {Nishino, Yoshinori and Eltsov, Mikhail and Joti, Yasumasa and Ito, Kazuki and Takata, Hideaki and Takahashi, Yukio and Hihara, Saera and Frangakis, Achilleas S. and Imamoto, Naoko and Ishikawa, Tetsuya and Maeshima, Kazuhiro},
  month = apr,
  year = {2012},
  keywords = {chromosome structure,30‐nm chromatin fibre,cryo‐EM,fractal structure,X‐ray sacattering},
  pages = {1644-1653},
  file = {/home/bbeltr1/Documents/paper-collection/MaeshimaK/Nishino et al_2012_Human mitotic chromosomes consist predominantly of irregularly folded.pdf;/home/bbeltr1/Documents/zotero/storage/JILSCE2Z/1644.html},
  pmid = {22343941}
}

@article{joti2012,
  title = {Chromosomes without a 30-Nm Chromatin Fiber},
  volume = {3},
  issn = {1949-1034},
  abstract = {How is a long strand of genomic DNA packaged into a mitotic chromosome or nucleus? The nucleosome fiber (beads-on-a-string), in which DNA is wrapped around core histones, has long been assumed to be folded into a 30-nm chromatin fiber, and a further helically folded larger fiber. However, when frozen hydrated human mitotic cells were observed using cryoelectron microscopy, no higher-order structures that included 30-nm chromatin fibers were found. To investigate the bulk structure of mitotic chromosomes further, we performed small-angle X-ray scattering (SAXS), which can detect periodic structures in noncrystalline materials in solution. The results were striking: no structural feature larger than 11 nm was detected, even at a chromosome-diameter scale ( 1 {$\mu$}m). We also found a similar scattering pattern in interphase nuclei of HeLa cells in the range up to 275 nm. Our findings suggest a common structural feature in interphase and mitotic chromatins: compact and irregular folding of nucleosome fibers occurs without a 30-nm chromatin structure.},
  number = {5},
  journal = {Nucleus},
  doi = {10.4161/nucl.21222},
  author = {Joti, Yasumasa and Hikima, Takaaki and Nishino, Yoshinori and Kamada, Fukumi and Hihara, Saera and Takata, Hideaki and Ishikawa, Tetsuya and Maeshima, Kazuhiro},
  month = sep,
  year = {2012},
  keywords = {chromatin,30-nm chromatin fiber,cryo-EM,fractal nature,interphase nuclei,irregular folding,mitotic chromosomes,X-ray scattering},
  pages = {404-410},
  file = {/home/bbeltr1/Documents/paper-collection/MaeshimaK/Joti et al_2012_Chromosomes without a 30-nm chromatin fiber.pdf;/home/bbeltr1/Documents/zotero/storage/IWBYUE9M/nucl.html},
  pmid = {22825571}
}

@article{maeshima2014,
  title = {Chromatin as Dynamic 10-Nm Fibers},
  volume = {123},
  issn = {0009-5915, 1432-0886},
  abstract = {Since Flemming described a nuclear substance in the nineteenth century and named it ``chromatin,'' this substance has fascinated biologists. What is the structure of chromatin? DNA is wrapped around core histones, forming a nucleosome fiber (10-nm fiber). This fiber has long been assumed to fold into a 30-nm chromatin fiber and subsequently into helically folded larger fibers or radial loops. However, several recent studies, including our cryo-EM and X-ray scattering analyses, demonstrated that chromatin is composed of irregularly folded 10-nm fibers, without 30-nm chromatin fibers, in interphase chromatin and mitotic chromosomes. This irregular folding implies a chromatin state that is physically less constrained, which could be more dynamic compared with classical regular helical folding structures. Consistent with this, recently, we uncovered by single nucleosome imaging large nucleosome fluctuations in living mammalian cells ({$\sim$}50 nm/30 ms). Subsequent computational modeling suggested that nucleosome fluctuation increases chromatin accessibility, which is advantageous for many ``target searching'' biological processes such as transcriptional regulation. Therefore, this review provides a novel view on chromatin structure in which chromatin consists of dynamic and disordered 10-nm fibers.},
  language = {en},
  number = {3},
  journal = {Chromosoma},
  doi = {10.1007/s00412-014-0460-2},
  author = {Maeshima, Kazuhiro and Imai, Ryosuke and Tamura, Sachiko and Nozaki, Tadasu},
  month = jun,
  year = {2014},
  pages = {225-237},
  file = {/home/bbeltr1/Documents/paper-collection/NozakiT/Maeshima et al_2014_Chromatin as dynamic 10-nm fibers.pdf;/home/bbeltr1/Documents/zotero/storage/TAY4RHBL/s00412-014-0460-2.html}
}

@article{mehraeen2008,
  title = {End-to-End Distribution for a Wormlike Chain in Arbitrary Dimensions},
  volume = {77},
  issn = {1539-3755, 1550-2376},
  language = {en},
  number = {6},
  journal = {Physical Review E},
  doi = {10.1103/PhysRevE.77.061803},
  author = {Mehraeen, Shafigh and Sudhanshu, Bariz and Koslover, Elena F. and Spakowitz, Andrew J.},
  month = jun,
  year = {2008},
  file = {/home/bbeltr1/Documents/paper-collection/SpakowitzA/Mehraeen et al_2008_End-to-end distribution for a wormlike chain in arbitrary dimensions.pdf}
}

@book{doi2007,
  address = {Oxford},
  series = {International Series of Monographs on Physics},
  title = {The Theory of Polymer Dynamics},
  isbn = {978-0-19-852033-7},
  language = {eng},
  number = {73},
  publisher = {{Clarendon Press}},
  author = {Doi, Masao and Edwards, Samuel F.},
  year = {2007},
  file = {/home/bbeltr1/Documents/paper-collection/EdwardsS/Doi_Edwards_2007_The theory of polymer dynamics.djvu;/home/bbeltr1/Documents/paper-collection/EdwardsS/Doi_Edwards_2007_The theory of polymer dynamics.pdf},
  note = {OCLC: 845169495}
}

@article{pierro2016,
  title = {Transferable Model for Chromosome Architecture},
  volume = {113},
  copyright = {\textcopyright{}  . http://www.pnas.org/site/misc/userlicense.xhtml},
  issn = {0027-8424, 1091-6490},
  abstract = {In vivo, the human genome folds into a characteristic ensemble of 3D structures. The mechanism driving the folding process remains unknown. We report a theoretical model for chromatin (Minimal Chromatin Model) that explains the folding of interphase chromosomes and generates chromosome conformations consistent with experimental data. The energy landscape of the model was derived by using the maximum entropy principle and relies on two experimentally derived inputs: a classification of loci into chromatin types and a catalog of the positions of chromatin loops. First, we trained our energy function using the Hi-C contact map of chromosome 10 from human GM12878 lymphoblastoid cells. Then, we used the model to perform molecular dynamics simulations producing an ensemble of 3D structures for all GM12878 autosomes. Finally, we used these 3D structures to generate contact maps. We found that simulated contact maps closely agree with experimental results for all GM12878 autosomes. The ensemble of structures resulting from these simulations exhibited unknotted chromosomes, phase separation of chromatin types, and a tendency for open chromatin to lie at the periphery of chromosome territories.},
  language = {en},
  number = {43},
  journal = {PNAS},
  doi = {10.1073/pnas.1613607113},
  author = {Pierro, Michele Di and Zhang, Bin and Aiden, Erez Lieberman and Wolynes, Peter G. and Onuchic, Jos\'e N.},
  month = oct,
  year = {2016},
  keywords = {Hi-C,genome architecture,human genome,maximum entropy,molecular dynamics},
  pages = {12168-12173},
  file = {/home/bbeltr1/Documents/paper-collection/OnuchicJ/Pierro et al_2016_Transferable model for chromosome architecture.pdf;/home/bbeltr1/Documents/zotero/storage/Q2LFF6DB/12168.html},
  pmid = {27688758}
}

@article{pierro2017,
  title = {De Novo Prediction of Human Chromosome Structures: {{Epigenetic}} Marking Patterns Encode Genome Architecture},
  volume = {114},
  copyright = {Copyright \textcopyright{} 2017 the Author(s). Published by PNAS.. This open access article is distributed under Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND).},
  issn = {0027-8424, 1091-6490},
  shorttitle = {De Novo Prediction of Human Chromosome Structures},
  abstract = {Inside the cell nucleus, genomes fold into organized structures that are characteristic of cell type. Here, we show that this chromatin architecture can be predicted de novo using epigenetic data derived from chromatin immunoprecipitation-sequencing (ChIP-Seq). We exploit the idea that chromosomes encode a 1D sequence of chromatin structural types. Interactions between these chromatin types determine the 3D structural ensemble of chromosomes through a process similar to phase separation. First, a neural network is used to infer the relation between the epigenetic marks present at a locus, as assayed by ChIP-Seq, and the genomic compartment in which those loci reside, as measured by DNA-DNA proximity ligation (Hi-C). Next, types inferred from this neural network are used as an input to an energy landscape model for chromatin organization [Minimal Chromatin Model (MiChroM)] to generate an ensemble of 3D chromosome conformations at a resolution of 50 kilobases (kb). After training the model, dubbed Maximum Entropy Genomic Annotation from Biomarkers Associated to Structural Ensembles (MEGABASE), on odd-numbered chromosomes, we predict the sequences of chromatin types and the subsequent 3D conformational ensembles for the even chromosomes. We validate these structural ensembles by using ChIP-Seq tracks alone to predict Hi-C maps, as well as distances measured using 3D fluorescence in situ hybridization (FISH) experiments. Both sets of experiments support the hypothesis of phase separation being the driving process behind compartmentalization. These findings strongly suggest that epigenetic marking patterns encode sufficient information to determine the global architecture of chromosomes and that de novo structure prediction for whole genomes may be increasingly possible.},
  language = {en},
  number = {46},
  journal = {PNAS},
  doi = {10.1073/pnas.1714980114},
  author = {Pierro, Michele Di and Cheng, Ryan R. and Aiden, Erez Lieberman and Wolynes, Peter G. and Onuchic, Jos\'e N.},
  month = nov,
  year = {2017},
  keywords = {Hi-C,energy landscape theory,epigenetics,genomic architecture,machine learning},
  pages = {12126-12131},
  file = {/home/bbeltr1/Documents/paper-collection/OnuchicJ/Pierro et al_2017_De novo prediction of human chromosome structures.pdf;/home/bbeltr1/Documents/zotero/storage/D6SC2X9M/12126.html},
  pmid = {29087948}
}

@article{rousseau2011,
  title = {Three-Dimensional Modeling of Chromatin Structure from Interaction Frequency Data Using {{Markov}} Chain {{Monte Carlo}} Sampling},
  volume = {12},
  issn = {1471-2105},
  abstract = {Long-range interactions between regulatory DNA elements such as enhancers, insulators and promoters play an important role in regulating transcription. As chromatin contacts have been found throughout the human genome and in different cell types, spatial transcriptional control is now viewed as a general mechanism of gene expression regulation. Chromosome Conformation Capture Carbon Copy (5C) and its variant Hi-C are techniques used to measure the interaction frequency (IF) between specific regions of the genome. Our goal is to use the IF data generated by these experiments to computationally model and analyze three-dimensional chromatin organization.},
  journal = {BMC Bioinformatics},
  doi = {10.1186/1471-2105-12-414},
  author = {Rousseau, Mathieu and Fraser, James and Ferraiuolo, Maria A. and Dostie, Jos\'ee and Blanchette, Mathieu},
  month = oct,
  year = {2011},
  keywords = {Base Density,HoxA Cluster,Interaction Frequency,Markov Chain Monte Carlo,Markov Chain Monte Carlo Sampling},
  pages = {414},
  file = {/home/bbeltr1/Documents/paper-collection/BlanchetteM/Rousseau et al_2011_Three-dimensional modeling of chromatin structure from interaction frequency.pdf;/home/bbeltr1/Documents/zotero/storage/HJUKGFY9/1471-2105-12-414.html}
}

@article{wang2015,
  title = {Inferential Modeling of {{3D}} Chromatin Structure},
  volume = {43},
  issn = {0305-1048},
  abstract = {For eukaryotic cells, the biological processes involving regulatory DNA elements play an important role in cell cycle. Understanding 3D spatial arrangements of chromosomes and revealing long-range chromatin interactions are critical to decipher these biological processes. In recent years, chromosome conformation capture (3C) related techniques have been developed to measure the interaction frequencies between long-range genome loci, which have provided a great opportunity to decode the 3D organization of the genome. In this paper, we develop a new Bayesian framework to derive the 3D architecture of a chromosome from 3C-based data. By modeling each chromosome as a polymer chain, we define the conformational energy based on our current knowledge on polymer physics and use it as prior information in the Bayesian framework. We also propose an expectation-maximization (EM) based algorithm to estimate the unknown parameters of the Bayesian model and infer an ensemble of chromatin structures based on interaction frequency data. We have validated our Bayesian inference approach through cross-validation and verified the computed chromatin conformations using the geometric constraints derived from fluorescence in situ hybridization (FISH) experiments. We have further confirmed the inferred chromatin structures using the known genetic interactions derived from other studies in the literature. Our test results have indicated that our Bayesian framework can compute an accurate ensemble of 3D chromatin conformations that best interpret the distance constraints derived from 3C-based data and also agree with other sources of geometric constraints derived from experimental evidence in the previous studies. The source code of our approach can be found in https://github.com/wangsy11/InfMod3DGen.},
  number = {8},
  journal = {Nucleic Acids Res},
  doi = {10.1093/nar/gkv100},
  author = {Wang, Siyu and Xu, Jinbo and Zeng, Jianyang},
  month = apr,
  year = {2015},
  pages = {e54},
  file = {/home/bbeltr1/Documents/paper-collection/ZengJ/Wang et al_2015_Inferential modeling of 3D chromatin structure.pdf},
  pmid = {25690896},
  pmcid = {PMC4417147}
}

@article{xie2017,
  title = {Structural {{Modeling}} of {{Chromatin Integrates Genome Features}} and {{Reveals Chromosome Folding Principle}}},
  volume = {7},
  copyright = {2017 The Author(s)},
  issn = {2045-2322},
  abstract = {How chromosomes fold into 3D structures and how genome functions are affected or even controlled by their spatial organization remain challenging questions. Hi-C experiment has provided important structural insights for chromosome, and Hi-C data are used here to construct the 3D chromatin structure which are characterized by two spatially segregated chromatin compartments A and B. By mapping a plethora of genome features onto the constructed 3D chromatin model, we show vividly the close connection between genome properties and the spatial organization of chromatin. We are able to dissect the whole chromatin into two types of chromatin domains which have clearly different Hi-C contact patterns as well as different sizes of chromatin loops. The two chromatin types can be respectively regarded as the basic units of chromatin compartments A and B, and also spatially segregate from each other as the two chromatin compartments. Therefore, the chromatin loops segregate in the space according to their sizes, suggesting the excluded volume or entropic effect in chromatin compartmentalization as well as chromosome positioning. Taken together, these results provide clues to the folding principles of chromosomes, their spatial organization, and the resulted clustering of many genome features in the 3D space.},
  language = {en},
  number = {1},
  journal = {Scientific Reports},
  doi = {10.1038/s41598-017-02923-6},
  author = {Xie, Wen Jun and Meng, Luming and Liu, Sirui and Zhang, Ling and Cai, Xiaoxia and Gao, Yi Qin},
  month = jun,
  year = {2017},
  pages = {2818},
  file = {/home/bbeltr1/Documents/paper-collection/GaoY/Xie et al_2017_Structural Modeling of Chromatin Integrates Genome Features and Reveals.pdf;/home/bbeltr1/Documents/zotero/storage/HKYXH7WU/s41598-017-02923-6.html}
}

@article{mirny2011,
  title = {The Fractal Globule as a Model of Chromatin Architecture in the Cell},
  volume = {19},
  issn = {0967-3849, 1573-6849},
  abstract = {The fractal globule is a compact polymer state that emerges during polymer condensation as a result of topological constraints which prevent one region of the chain from passing across another one. This long-lived intermediate state was introduced in 1988 (Grosberg et al. 1988) and has not been observed in experiments or simulations until recently (Lieberman-Aiden et al. 2009). Recent characterization of human chromatin using a novel chromosome conformational capture technique brought the fractal globule into the spotlight as a structural model of human chromosome on the scale of up to 10 Mb (Lieberman-Aiden et al. 2009). Here, we present the concept of the fractal globule, comparing it to other states of a polymer and focusing on its properties relevant for the biophysics of chromatin. We then discuss properties of the fractal globule that make it an attractive model for chromatin organization inside a cell. Next, we connect the fractal globule to recent studies that emphasize topological constraints as a primary factor driving formation of chromosomal territories. We discuss how theoretical predictions, made on the basis of the fractal globule model, can be tested experimentally. Finally, we discuss whether fractal globule architecture can be relevant for chromatin packing in other organisms such as yeast and bacteria.},
  language = {en},
  number = {1},
  journal = {Chromosome Res},
  doi = {10.1007/s10577-010-9177-0},
  author = {Mirny, Leonid A.},
  month = jan,
  year = {2011},
  pages = {37-51},
  file = {/home/bbeltr1/Documents/paper-collection/MirnyL/Mirny_2011_The fractal globule as a model of chromatin architecture in the cell.pdf;/home/bbeltr1/Documents/zotero/storage/DESM28LP/10.html}
}

@article{varoquaux2014,
  title = {A Statistical Approach for Inferring the {{3D}} Structure of the Genome},
  volume = {30},
  issn = {1367-4803},
  abstract = {Abstract.  Motivation: Recent technological advances allow the measurement, in a single Hi-C experiment, of the frequencies of physical contacts among pairs of},
  language = {en},
  number = {12},
  journal = {Bioinformatics},
  doi = {10.1093/bioinformatics/btu268},
  author = {Varoquaux, Nelle and Ay, Ferhat and Noble, William Stafford and Vert, Jean-Philippe},
  month = jun,
  year = {2014},
  pages = {i26-i33},
  file = {/home/bbeltr1/Documents/paper-collection/VertJ/Varoquaux et al_2014_A statistical approach for inferring the 3D structure of the genome.pdf;/home/bbeltr1/Documents/zotero/storage/AEHXDLUL/385087.html}
}

@article{grigoryev2009,
  title = {Evidence for Heteromorphic Chromatin Fibers from Analysis of Nucleosome Interactions},
  volume = {106},
  copyright = {\textcopyright{} 2009},
  issn = {0027-8424, 1091-6490},
  abstract = {The architecture of the chromatin fiber, which determines DNA accessibility for transcription and other template-directed biological processes, remains unknown. Here we investigate the internal organization of the 30-nm chromatin fiber, combining Monte Carlo simulations of nucleosome chain folding with EM-assisted nucleosome interaction capture (EMANIC). We show that at physiological concentrations of monovalent ions, linker histones lead to a tight 2-start zigzag dominated by interactions between alternate nucleosomes (i {$\pm$} 2) and sealed by histone N-tails. Divalent ions further compact the fiber by promoting bending in some linker DNAs and hence raising sequential nucleosome interactions (i {$\pm$} 1). Remarkably, both straight and bent linker DNA conformations are retained in the fully compact chromatin fiber as inferred from both EMANIC and modeling. This conformational variability is energetically favorable as it helps accommodate DNA crossings within the fiber axis. Our results thus show that the 2-start zigzag topology and the type of linker DNA bending that defines solenoid models may be simultaneously present in a structurally heteromorphic chromatin fiber with uniform 30 nm diameter. Our data also suggest that dynamic linker DNA bending by linker histones and divalent cations in vivo may mediate the transition between tight nucleosome packing within discrete 30-nm fibers and self-associated higher-order chromosomal forms.},
  language = {en},
  number = {32},
  journal = {PNAS},
  doi = {10.1073/pnas.0903280106},
  author = {Grigoryev, Sergei A. and Arya, Gaurav and Correll, Sarah and Woodcock, Christopher L. and Schlick, Tamar},
  month = aug,
  year = {2009},
  keywords = {chromatin structure,Monte Carlo simulations,linker histone,electron microscopy,mesoscopic modeling},
  pages = {13317-13322},
  file = {/home/bbeltr1/Documents/paper-collection/SchlickT/Grigoryev et al_2009_Evidence for heteromorphic chromatin fibers from analysis of nucleosome.pdf;/home/bbeltr1/Documents/zotero/storage/DRZWMJGY/13317.html},
  pmid = {19651606}
}

@article{brackley2018,
  title = {Extrusion without a Motor: A New Take on the Loop Extrusion Model of Genome Organization},
  volume = {9},
  issn = {1949-1034, 1949-1042},
  shorttitle = {Extrusion without a Motor},
  language = {en},
  number = {1},
  journal = {Nucleus},
  doi = {10.1080/19491034.2017.1421825},
  author = {Brackley, C. A. and Johnson, J. and Michieletto, D. and Morozov, A. N. and Nicodemi, M. and Cook, P. R. and Marenduzzo, D.},
  month = jan,
  year = {2018},
  pages = {95-103},
  file = {/home/bbeltr1/Documents/paper-collection/MarenduzzoD/Brackley et al_2018_Extrusion without a motor.pdf}
}

@article{cortini2018,
  title = {Theoretical Principles of Transcription Factor Traffic on Folded Chromatin},
  volume = {9},
  copyright = {2018 The Author(s)},
  issn = {2041-1723},
  abstract = {How transcription factors find their targets in vivo is still poorly understood. Here the authors use molecular dynamics simulations to investigate how transcription factors diffuse on chromatin, providing a theoretical framework for understanding the key role of genome conformation in this process.},
  language = {en},
  number = {1},
  journal = {Nature Communications},
  doi = {10.1038/s41467-018-04130-x},
  author = {Cortini, Ruggero and Filion, Guillaume J.},
  month = apr,
  year = {2018},
  pages = {1740},
  file = {/home/bbeltr1/Documents/paper-collection/FilionG/Cortini_Filion_2018_Theoretical principles of transcription factor traffic on folded chromatin.pdf;/home/bbeltr1/Documents/zotero/storage/SWPH7YDP/s41467-018-04130-x.html}
}

@article{nora2017,
  title = {Targeted {{Degradation}} of {{CTCF Decouples Local Insulation}} of {{Chromosome Domains}} from {{Genomic Compartmentalization}}},
  volume = {169},
  issn = {00928674},
  abstract = {The molecular mechanisms underlying folding of mammalian chromosomes remain poorly understood. The transcription factor CTCF is a candidate regulator of chromosomal structure. Using the auxin-inducible degron system in mouse embryonic stem cells, we show that CTCF is absolutely and dose-dependently required for looping between CTCF target sites and insulation of topologically associating domains (TADs). Restoring CTCF reinstates proper architecture on altered chromosomes, indicating a powerful instructive function for CTCF in chromatin folding. CTCF remains essential for TAD organization in non-dividing cells. Surprisingly, active and inactive genome compartments remain properly segregated upon CTCF depletion, revealing that compartmentalization of mammalian chromosomes emerges independently of proper insulation of TADs. Furthermore, our data support that CTCF mediates transcriptional insulator function through enhancer blocking but not as a direct barrier to heterochromatin spreading. Beyond defining the functions of CTCF in chromosome folding, these results provide new fundamental insights into the rules governing mammalian genome organization.},
  language = {en},
  number = {5},
  journal = {Cell},
  doi = {10.1016/j.cell.2017.05.004},
  author = {Nora, Elph\`ege P. and Goloborodko, Anton and Valton, Anne-Laure and Gibcus, Johan H. and Uebersohn, Alec and Abdennur, Nezar and Dekker, Job and Mirny, Leonid A. and Bruneau, Benoit G.},
  month = may,
  year = {2017},
  pages = {930-944.e22},
  file = {/home/bbeltr1/Documents/paper-collection/BruneauB/Nora et al_2017_Targeted Degradation of CTCF Decouples Local Insulation of Chromosome Domains.pdf}
}

@article{dewit2015,
  title = {{{CTCF Binding Polarity Determines Chromatin Looping}}},
  volume = {60},
  issn = {10972765},
  language = {en},
  number = {4},
  journal = {Molecular Cell},
  doi = {10.1016/j.molcel.2015.09.023},
  author = {{de Wit}, Elzo and Vos, Erica S.M. and Holwerda, Sjoerd J.B. and {Valdes-Quezada}, Christian and Verstegen, Marjon J.A.M. and Teunissen, Hans and Splinter, Erik and Wijchers, Patrick J. and Krijger, Peter H.L. and {de Laat}, Wouter},
  month = nov,
  year = {2015},
  pages = {676-684},
  file = {/home/bbeltr1/Documents/paper-collection/de LaatW/de Wit et al_2015_CTCF Binding Polarity Determines Chromatin Looping.pdf}
}

@article{supek2015,
  title = {Differential {{DNA}} Mismatch Repair Underlies Mutation Rate Variation across the Human Genome},
  volume = {521},
  copyright = {2015 Nature Publishing Group},
  issn = {1476-4687},
  abstract = {Cancer genome sequencing has revealed considerable variation in somatic mutation rates across the human genome, with mutation rates elevated in heterochromatic late replicating regions and reduced in early replicating euchromatin1,2,3,4,5. Multiple mechanisms have been suggested to underlie this2,6,7,8,9,10, but the actual cause is unknown. Here we identify variable DNA mismatch repair (MMR) as the basis of this variation. Analysing {$\sim$}17 million single-nucleotide variants from the genomes of 652 tumours, we show that regional autosomal mutation rates at megabase resolution are largely stable across cancer types, with differences related to changes in replication timing and gene expression. However, mutations arising after the inactivation of MMR are no longer enriched in late replicating heterochromatin relative to early replicating euchromatin. Thus, differential DNA repair and not differential mutation supply is the primary cause of the large-scale regional mutation rate variation across the human genome.},
  language = {en},
  number = {7550},
  journal = {Nature},
  doi = {10.1038/nature14173},
  author = {Supek, Fran and Lehner, Ben},
  month = may,
  year = {2015},
  pages = {81-84},
  file = {/home/bbeltr1/Documents/paper-collection/LehnerB/Supek_Lehner_2015_Differential DNA mismatch repair underlies mutation rate variation across the.pdf;/home/bbeltr1/Documents/zotero/storage/RBC8ZX6Z/nature14173.html}
}

@article{iwafuchi-doi2014,
  title = {Pioneer Transcription Factors in Cell Reprogramming},
  volume = {28},
  issn = {0890-9369, 1549-5477},
  abstract = {A subset of eukaryotic transcription factors possesses the remarkable ability to reprogram one type of cell into another. The transcription factors that reprogram cell fate are invariably those that are crucial for the initial cell programming in embryonic development. To elicit cell programming or reprogramming, transcription factors must be able to engage genes that are developmentally silenced and inappropriate for expression in the original cell. Developmentally silenced genes are typically embedded in ``closed'' chromatin that is covered by nucleosomes and not hypersensitive to nuclease probes such as DNase I. Biochemical and genomic studies have shown that transcription factors with the highest reprogramming activity often have the special ability to engage their target sites on nucleosomal DNA, thus behaving as ``pioneer factors'' to initiate events in closed chromatin. Other reprogramming factors appear dependent on pioneer factors for engaging nucleosomes and closed chromatin. However, certain genomic domains in which nucleosomes are occluded by higher-order chromatin structures, such as in heterochromatin, are resistant to pioneer factor binding. Understanding the means by which pioneer factors can engage closed chromatin and how heterochromatin can prevent such binding promises to advance our ability to reprogram cell fates at will and is the topic of this review.},
  language = {en},
  number = {24},
  journal = {Genes Dev.},
  doi = {10.1101/gad.253443.114},
  author = {{Iwafuchi-Doi}, Makiko and Zaret, Kenneth S.},
  month = dec,
  year = {2014},
  keywords = {development,chromatin,nucleosome,pioneer transcription factor,reprogramming,transdifferentiation},
  pages = {2679-2692},
  file = {/home/bbeltr1/Documents/paper-collection/ZaretK/Iwafuchi-Doi_Zaret_2014_Pioneer transcription factors in cell reprogramming.pdf},
  pmid = {25512556}
}

@article{nozaki2017,
  title = {Dynamic {{Organization}} of {{Chromatin Domains Revealed}} by {{Super}}-{{Resolution Live}}-{{Cell Imaging}}},
  volume = {67},
  issn = {1097-2765},
  abstract = {Summary
The eukaryotic genome is organized within cells as chromatin. For proper information output, higher-order chromatin structures can be regulated dynamically. How such structures form and behave in various cellular processes remains unclear. Here, by combining super-resolution imaging (photoactivated localization microscopy [PALM]) and single-nucleosome tracking, we developed a nuclear imaging system to visualize the higher-order structures along with their dynamics in live mammalian cells. We demonstrated that nucleosomes form compact domains with a peak diameter of {$\sim$}160~nm and move coherently in live cells. The heterochromatin-rich regions showed more domains and less movement. With cell differentiation, the domains became more apparent, with reduced dynamics. Furthermore, various perturbation experiments indicated that they are organized by a combination of factors, including cohesin and nucleosome-nucleosome interactions. Notably, we observed the domains during mitosis, suggesting that they act as building blocks of chromosomes and may serve as information units throughout the cell cycle.},
  number = {2},
  journal = {Molecular Cell},
  doi = {10.1016/j.molcel.2017.06.018},
  author = {Nozaki, Tadasu and Imai, Ryosuke and Tanbo, Mai and Nagashima, Ryosuke and Tamura, Sachiko and Tani, Tomomi and Joti, Yasumasa and Tomita, Masaru and Hibino, Kayo and Kanemaki, Masato T. and Wendt, Kerstin S. and Okada, Yasushi and Nagai, Takeharu and Maeshima, Kazuhiro},
  month = jul,
  year = {2017},
  keywords = {chromatin,chromatin domain,chromatin dynamics,chromosome,PALM,single-nucleosome tracking},
  pages = {282-293.e7},
  file = {/home/bbeltr1/Documents/paper-collection/MaeshimaK/Nozaki et al_2017_Dynamic Organization of Chromatin Domains Revealed by Super-Resolution.pdf;/home/bbeltr1/Documents/zotero/storage/8WN28594/S1097276517304458.html}
}

@article{ricci2015,
  title = {Chromatin {{Fibers Are Formed}} by {{Heterogeneous Groups}} of {{Nucleosomes In Vivo}}},
  volume = {160},
  issn = {0092-8674, 1097-4172},
  language = {English},
  number = {6},
  journal = {Cell},
  doi = {10.1016/j.cell.2015.01.054},
  author = {Ricci, Maria Aurelia and Manzo, Carlo and {Garc\'ia-Parajo}, Mar\'ia Filomena and Lakadamyali, Melike and Cosma, Maria Pia},
  month = mar,
  year = {2015},
  pages = {1145-1158},
  file = {/home/bbeltr1/Documents/paper-collection/CosmaM/Ricci et al_2015_Chromatin Fibers Are Formed by Heterogeneous Groups of Nucleosomes In Vivo.pdf;/home/bbeltr1/Documents/zotero/storage/DAW5H4MG/S0092-8674(15)00132-4.html},
  pmid = {25768910}
}

@article{daban2015,
  title = {Stacked Thin Layers of Metaphase Chromatin Explain the Geometry of Chromosome Rearrangements and Banding},
  volume = {5},
  copyright = {2015 Nature Publishing Group},
  issn = {2045-2322},
  abstract = {The three-dimensional organization of tightly condensed chromatin within metaphase chromosomes has been one of the most challenging problems in structural biology since the discovery of the nucleosome. This study shows that chromosome images obtained from typical banded karyotypes and from different multicolour cytogenetic analyses can be used to gain information about the internal structure of chromosomes. Chromatin bands and the connection surfaces in sister chromatid exchanges and in cancer translocations are planar and orthogonal to the chromosome axis. Chromosome stretching produces band splitting and even the thinnest bands are orthogonal and well defined, indicating that short stretches of DNA can occupy completely the chromosome cross-section. These observations impose strong physical constraints on models that attempt to explain chromatin folding in chromosomes. The thin-plate model, which consists of many stacked layers of planar chromatin perpendicular to the chromosome axis, is compatible with the observed orientation of bands, with the existence of thin bands, and with band splitting; it is also compatible with the orthogonal orientation and planar geometry of the connection surfaces in chromosome rearrangements. The results obtained provide a consistent interpretation of the chromosome structural properties that are used in clinical cytogenetics for the diagnosis of hereditary diseases and cancers.},
  language = {en},
  journal = {Scientific Reports},
  doi = {10.1038/srep14891},
  author = {Daban, Joan-Ramon},
  month = oct,
  year = {2015},
  pages = {14891},
  file = {/home/bbeltr1/Documents/paper-collection/DabanJ/Daban_2015_Stacked thin layers of metaphase chromatin explain the geometry of chromosome.pdf;/home/bbeltr1/Documents/zotero/storage/WC6LNR7W/srep14891.html}
}

@article{meng2017,
  title = {Emerging {{Roles}} of {{Transcriptional Enhancers In Chromatin Looping And Promoter}}-{{Proximal Pausing Of RNA Polymerase II}}},
  issn = {0021-9258, 1083-351X},
  language = {en},
  journal = {J. Biol. Chem.},
  doi = {10.1074/jbc.R117.813485},
  author = {Meng, Huan and Bartholomew, Blaine},
  month = nov,
  year = {2017},
  pages = {jbc.R117.813485},
  file = {/home/bbeltr1/Documents/paper-collection/BartholomewB/Meng_Bartholomew_2017_Emerging Roles of Transcriptional Enhancers In Chromatin Looping And.pdf;/home/bbeltr1/Documents/zotero/storage/GV3GEYD2/jbc.R117.813485.html},
  pmid = {29187597}
}

@article{cutter2015a,
  title = {A {{Brief Review}} of {{Nucleosome Structure}}},
  volume = {589},
  issn = {0014-5793},
  abstract = {The nucleosomal subunit organization of chromatin provides a multitude of functions. Nucleosomes elicit an initial \textasciitilde{}7-fold linear compaction of genomic DNA. They provide a critical mechanism for stable repression of genes and other DNA-dependent activities by restricting binding of trans-acting factors to cognate DNA sequences. Conversely they are engineered to be nearly meta-stable and disassembled (and reassembled) in a facile manner to allow rapid access to the underlying DNA during processes such as transcription, replication and DNA repair. Nucleosomes protect the genome from DNA damaging agents and provide a lattice onto which a myriad of epigenetic signals are deposited. Moreover, vast strings of nucleosomes provide a framework for assembly of the chromatin fiber and higher-order chromatin structures. Thus, in order to provide a foundation for understanding these functions, we present a review of the basic elements of nucleosome structure and stability, including the association of linker histones.},
  number = {20 0 0},
  journal = {FEBS Lett},
  doi = {10.1016/j.febslet.2015.05.016},
  author = {Cutter, Amber and Hayes, Jeffrey J.},
  month = oct,
  year = {2015},
  pages = {2914-2922},
  file = {/home/bbeltr1/Documents/paper-collection/HayesJ/Cutter_Hayes_2015_A Brief Review of Nucleosome Structure.pdf},
  pmid = {25980611},
  pmcid = {PMC4598263}
}

@article{bednar2017,
  title = {Structure and {{Dynamics}} of a 197 Bp {{Nucleosome}} in {{Complex}} with {{Linker Histone H1}}},
  volume = {66},
  issn = {1097-2765},
  abstract = {Linker histones associate with nucleosomes to promote the formation of higher-order chromatin structure, but the underlying molecular details are unclear. We investigated the structure of a 197~bp nucleosome bearing symmetric 25~bp linker DNA arms in complex with vertebrate linker histone H1. We determined electron cryo-microscopy (cryo-EM) and crystal structures of unbound and H1-bound nucleosomes and validated these structures by site-directed protein cross-linking and hydroxyl radical footprinting experiments. Histone H1 shifts the conformational landscape of the nucleosome by drawing the two linkers together and reducing their flexibility. The H1 C-terminal domain (CTD) localizes primarily to a single linker, while the H1 globular domain contacts the nucleosome dyad and both linkers, associating more closely with the CTD-distal linker. These findings reveal that H1 imparts a strong degree of asymmetry to the nucleosome, which is likely to influence the assembly and architecture of higher-order structures.},
  language = {English},
  number = {3},
  journal = {Molecular Cell},
  doi = {10.1016/j.molcel.2017.04.012},
  author = {Bednar, Jan and {Garcia-Saez}, Isabel and Boopathi, Ramachandran and Cutter, Amber R. and Papai, Gabor and Reymer, Anna and Syed, Sajad H. and Lone, Imtiaz Nisar and Tonchev, Ognyan and Crucifix, Corinne and Menoni, Herv\'e and Papin, Christophe and Skoufias, Dimitrios A. and Kurumizaka, Hitoshi and Lavery, Richard and Hamiche, Ali and Hayes, Jeffrey J. and Schultz, Patrick and Angelov, Dimitar and Petosa, Carlo and Dimitrov, Stefan},
  month = may,
  year = {2017},
  keywords = {chromatin,nucleosome,linker histone,cryo-EM,histone H1,hydroxyl radical footprinting,protein-DNA crosslinking,X-ray crystallography},
  pages = {384-397.e8},
  file = {/home/bbeltr1/Documents/paper-collection/DimitrovS/Bednar et al_2017_Structure and Dynamics of a 197 bp Nucleosome in Complex with Linker Histone H1.pdf;/home/bbeltr1/Documents/zotero/storage/5RRY5LLG/S1097-2765(17)30268-X.html},
  pmid = {28475873}
}

@article{richmond2003,
  title = {The Structure of {{DNA}} in the Nucleosome Core},
  volume = {423},
  issn = {0028-0836, 1476-4687},
  language = {en},
  number = {6936},
  journal = {Nature},
  doi = {10.1038/nature01595},
  author = {Richmond, Timothy J. and Davey, Curt A.},
  month = may,
  year = {2003},
  pages = {145-150},
  file = {/home/bbeltr1/Documents/paper-collection/DaveyC/Richmond_Davey_2003_The structure of DNA in the nucleosome core.pdf}
}

@article{gaffney2012,
  title = {Controls of {{Nucleosome Positioning}} in the {{Human Genome}}},
  volume = {8},
  issn = {1553-7404},
  abstract = {Nucleosomes are important for gene regulation because their arrangement on the genome can control which proteins bind to DNA. Currently, few human nucleosomes are thought to be consistently positioned across cells; however, this has been difficult to assess due to the limited resolution of existing data. We performed paired-end sequencing of micrococcal nuclease-digested chromatin (MNase\textendash{}seq) from seven lymphoblastoid cell lines and mapped over 3.6 billion MNase\textendash{}seq fragments to the human genome to create the highest-resolution map of nucleosome occupancy to date in a human cell type. In contrast to previous results, we find that most nucleosomes have more consistent positioning than expected by chance and a substantial fraction (8.7\%) of nucleosomes have moderate to strong positioning. In aggregate, nucleosome sequences have 10 bp periodic patterns in dinucleotide frequency and DNase I sensitivity; and, across cells, nucleosomes frequently have translational offsets that are multiples of 10 bp. We estimate that almost half of the genome contains regularly spaced arrays of nucleosomes, which are enriched in active chromatin domains. Single nucleotide polymorphisms that reduce DNase I sensitivity can disrupt the phasing of nucleosome arrays, which indicates that they often result from positioning against a barrier formed by other proteins. However, nucleosome arrays can also be created by DNA sequence alone. The most striking example is an array of over 400 nucleosomes on chromosome 12 that is created by tandem repetition of sequences with strong positioning properties. In summary, a large fraction of nucleosomes are consistently positioned\textemdash{}in some regions because they adopt favored sequence positions, and in other regions because they are forced into specific arrangements by chromatin remodeling or DNA binding proteins.},
  language = {en},
  number = {11},
  journal = {PLOS Genetics},
  doi = {10.1371/journal.pgen.1003036},
  author = {Gaffney, Daniel J. and McVicker, Graham and Pai, Athma A. and {Fondufe-Mittendorf}, Yvonne N. and Lewellen, Noah and Michelini, Katelyn and Widom, Jonathan and Gilad, Yoav and Pritchard, Jonathan K.},
  month = nov,
  year = {2012},
  keywords = {Chromatin,Nucleosomes,DNA-binding proteins,Nucleosome mapping,Deoxyribonucleases,Genomic libraries,Human genomics,Transcription factors},
  pages = {e1003036},
  file = {/home/bbeltr1/Documents/paper-collection/PritchardJ/Gaffney et al_2012_Controls of Nucleosome Positioning in the Human Genome.pdf}
}

@article{gupta2008,
  title = {Predicting {{Human Nucleosome Occupancy}} from {{Primary Sequence}}},
  volume = {4},
  issn = {1553-7358},
  abstract = {Nucleosomes are the fundamental repeating unit of chromatin and comprise the structural building blocks of the living eukaryotic genome. Micrococcal nuclease (MNase) has long been used to delineate nucleosomal organization. Microarray-based nucleosome mapping experiments in yeast chromatin have revealed regularly-spaced translational phasing of nucleosomes. These data have been used to train computational models of sequence-directed nuclesosome positioning, which have identified ubiquitous strong intrinsic nucleosome positioning signals. Here, we successfully apply this approach to nucleosome positioning experiments from human chromatin. The predictions made by the human-trained and yeast-trained models are strongly correlated, suggesting a shared mechanism for sequence-based determination of nucleosome occupancy. In addition, we observed striking complementarity between classifiers trained on experimental data from weakly versus heavily digested MNase samples. In the former case, the resulting model accurately identifies nucleosome-forming sequences; in the latter, the classifier excels at identifying nucleosome-free regions. Using this model we are able to identify several characteristics of nucleosome-forming and nucleosome-disfavoring sequences. First, by combining results from each classifier applied de novo across the human ENCODE regions, the classifier reveals distinct sequence composition and periodicity features of nucleosome-forming and nucleosome-disfavoring sequences. Short runs of dinucleotide repeat appear as a hallmark of nucleosome-disfavoring sequences, while nucleosome-forming sequences contain short periodic runs of GC base pairs. Second, we show that nucleosome phasing is most frequently predicted flanking nucleosome-free regions. The results suggest that the major mechanism of nucleosome positioning in vivo is boundary-event-driven and affirm the classical statistical positioning theory of nucleosome organization.},
  language = {en},
  number = {8},
  journal = {PLOS Computational Biology},
  doi = {10.1371/journal.pcbi.1000134},
  author = {Gupta, Shobhit and Dennis, Jonathan and Thurman, Robert E. and Kingston, Robert and Stamatoyannopoulos, John A. and Noble, William Stafford},
  month = aug,
  year = {2008},
  keywords = {Chromatin,Histones,Nucleosomes,Sequence motif analysis,DNA sequence analysis,DNA transcription,Microarrays,Repeated sequences},
  pages = {e1000134},
  file = {/home/bbeltr1/Documents/paper-collection/NobleW/Gupta et al_2008_Predicting Human Nucleosome Occupancy from Primary Sequence.pdf;/home/bbeltr1/Documents/zotero/storage/LHZI2Q3X/article.html}
}

@article{kaplan2009,
  title = {The {{DNA}}-Encoded Nucleosome Organization of a Eukaryotic Genome},
  volume = {458},
  copyright = {2008 Nature Publishing Group},
  issn = {1476-4687},
  abstract = {Nucleosome organization is critical for gene regulation1. In living cells this organization is determined by multiple factors, including the action of chromatin remodellers2, competition with site-specific DNA-binding proteins3, and the DNA sequence preferences of the nucleosomes themselves4,5,6,7,8. However, it has been difficult to estimate the relative importance of each of these mechanisms in vivo7,9,10,11, because in vivo nucleosome maps reflect the combined action of all influencing factors. Here we determine the importance of nucleosome DNA sequence preferences experimentally by measuring the genome-wide occupancy of nucleosomes assembled on purified yeast genomic DNA. The resulting map, in which nucleosome occupancy is governed only by the intrinsic sequence preferences of nucleosomes, is similar to in vivo nucleosome maps generated in three different growth conditions. In vitro, nucleosome depletion is evident at many transcription factor binding sites and around gene start and end sites, indicating that nucleosome depletion at these sites in vivo is partly encoded in the genome. We confirm these results with a micrococcal nuclease-independent experiment that measures the relative affinity of nucleosomes for {$\sim$}40,000 double-stranded 150-base-pair oligonucleotides. Using our in vitro data, we devise a computational model of nucleosome sequence preferences that is significantly correlated with in vivo nucleosome occupancy in Caenorhabditis elegans. Our results indicate that the intrinsic DNA sequence preferences of nucleosomes have a central role in determining the organization of nucleosomes in vivo.},
  language = {en},
  number = {7236},
  journal = {Nature},
  doi = {10.1038/nature07667},
  author = {Kaplan, Noam and Moore, Irene K. and {Fondufe-Mittendorf}, Yvonne and Gossett, Andrea J. and Tillo, Desiree and Field, Yair and LeProust, Emily M. and Hughes, Timothy R. and Lieb, Jason D. and Widom, Jonathan and Segal, Eran},
  month = mar,
  year = {2009},
  pages = {362-366},
  file = {/home/bbeltr1/Documents/paper-collection/SegalE/Kaplan et al_2009_The DNA-encoded nucleosome organization of a eukaryotic genome.pdf;/home/bbeltr1/Documents/zotero/storage/YMS2H5SR/nature07667.html}
}

@article{chereji2018b,
  title = {Precise Genome-Wide Mapping of Single Nucleosomes and Linkers in Vivo},
  volume = {19},
  issn = {1474-760X},
  abstract = {We developed a chemical cleavage method that releases single nucleosome dyad-containing fragments, allowing us to precisely map both single nucleosomes and linkers with high accuracy genome-wide in yeast. Our single nucleosome positioning data reveal that nucleosomes occupy preferred positions that differ by integral multiples of the DNA helical repeat. By comparing nucleosome dyad positioning maps to existing genomic and transcriptomic data, we evaluated the contributions of sequence, transcription, and histones H1 and H2A.Z in defining the chromatin landscape. We present a biophysical model that neglects DNA sequence and shows that steric occlusion suffices to explain the salient features of nucleosome positioning.},
  journal = {Genome Biology},
  doi = {10.1186/s13059-018-1398-0},
  author = {Chereji, R{\u a}zvan V. and Ramachandran, Srinivas and Bryson, Terri D. and Henikoff, Steven},
  month = feb,
  year = {2018},
  keywords = {Biophysical modeling,Chemical cleavage mapping,Linker quantization},
  pages = {19},
  file = {/home/bbeltr1/Documents/paper-collection/HenikoffS/Chereji et al_2018_Precise genome-wide mapping of single nucleosomes and linkers in vivo.pdf;/home/bbeltr1/Documents/zotero/storage/CH4WWH6F/s13059-018-1398-0.html}
}

@article{flaus1996,
  title = {Mapping Nucleosome Position at Single Base-Pair Resolution by Using Site-Directed Hydroxyl Radicals.},
  volume = {93},
  issn = {0027-8424, 1091-6490},
  abstract = {A base-pair resolution method for determining nucleosome position in vitro has been developed to complement existing, less accurate methods. Cysteaminyl EDTA was tethered to a recombinant histone octamer via a mutant histone H4 with serine 47 replaced by cysteine. When assembled into nucleosome core particles, the DNA could be cut site specifically by hydroxyl radical-catalyzed chain scission by using the Fenton reaction. Strand cleavage occurs mainly at a single nucleotide close to the dyad axis ofthe core particle, and assignment of this location via the symmetry of the nucleosome allows base-pair resolution mapping of the histone octamer position on the DNA. The positions of the histone octamer and H3H4 tetramer were mapped on a 146-bp Lytechinus variegatus 5S rRNA sequence and a twofold-symmetric derivative. The weakness of translational determinants of nucleosome positioning relative to the overall affinity of the histone proteins for this DNA is clearly demonstrated. The predominant location of both histone octamer and H3H4 tetramer assembled on the 5S rDNA is off center. Shifting the nucleosome core particle position along DNA within a conserved rotational phase could be induced under physiologically relevant conditions. Since nucleosome shifting has important consequences for chromatin structure and gene regulation, an approach to the thermodynamic characterization of this movement is proposed. This mapping method is potentially adaptable for determining nucleosome position in chromatin in vivo.},
  language = {en},
  number = {4},
  journal = {Proceedings of the National Academy of Sciences},
  doi = {10.1073/pnas.93.4.1370},
  author = {Flaus, A. and Luger, K. and Tan, S. and Richmond, T. J.},
  month = feb,
  year = {1996},
  pages = {1370-1375},
  file = {/home/bbeltr1/Documents/paper-collection/RichmondT/Flaus et al_1996_Mapping nucleosome position at single base-pair resolution by using.pdf}
}

@article{zhou2015,
  title = {Structural {{Mechanisms}} of {{Nucleosome Recognition}} by {{Linker Histones}}},
  volume = {59},
  issn = {1097-2765},
  abstract = {Linker histones bind to the nucleosome and regulate the structure of chromatin and gene expression. Despite more than three decades of effort, the structural basis of nucleosome recognition by linker histones remains elusive. Here, we report the crystal structure of the globular domain of chicken linker histone H5 in complex with the nucleosome at 3.5 \AA{} resolution, which is validated using nuclear magnetic resonance spectroscopy. The globular domain sits on the dyad of the nucleosome and interacts with both DNA linkers. Our structure integrates results from mutation analyses and previous cross-linking and fluorescence recovery after photobleach experiments, and it helps resolve the long debate on structural mechanisms of nucleosome recognition by linker histones. The on-dyad binding mode of the H5 globular domain is different from the recently reported off-dyad binding mode of Drosophila linker histone H1. We demonstrate that linker histones with different binding modes could fold chromatin to form distinct higher-order structures.},
  language = {English},
  number = {4},
  journal = {Molecular Cell},
  doi = {10.1016/j.molcel.2015.06.025},
  author = {Zhou, Bing-Rui and Jiang, Jiansheng and Feng, Hanqiao and Ghirlando, Rodolfo and Xiao, T. Sam and Bai, Yawen},
  month = aug,
  year = {2015},
  keywords = {nucleosome structure},
  pages = {628-638},
  file = {/home/bbeltr1/Documents/paper-collection/BaiY/Zhou et al_2015_Structural Mechanisms of Nucleosome Recognition by Linker Histones.pdf;/home/bbeltr1/Documents/zotero/storage/YNXG73FQ/S1097-2765(15)00497-9.html},
  pmid = {26212454}
}

@article{dixon2016,
  title = {Chromatin {{Domains}}: {{The Unit}} of {{Chromosome Organization}}},
  volume = {62},
  issn = {1097-2765},
  shorttitle = {Chromatin {{Domains}}},
  language = {English},
  number = {5},
  journal = {Molecular Cell},
  doi = {10.1016/j.molcel.2016.05.018},
  author = {Dixon, Jesse R. and Gorkin, David U. and Ren, Bing},
  month = jun,
  year = {2016},
  pages = {668-680},
  file = {/home/bbeltr1/Documents/paper-collection/RenB/Dixon et al_2016_Chromatin Domains.pdf;/home/bbeltr1/Documents/zotero/storage/F2YM6CI4/S1097-2765(16)30181-2.html}
}

@article{busslinger2017,
  title = {Cohesin Is Positioned in Mammalian Genomes by Transcription, {{CTCF}} and {{Wapl}}},
  volume = {544},
  copyright = {2017 Nature Publishing Group},
  issn = {1476-4687},
  abstract = {Mammalian genomes are spatially organized by CCCTC-binding factor (CTCF) and cohesin into chromatin loops1,2 and topologically associated domains3,4,5,6, which have important roles in gene regulation1,2,4,5,7 and recombination7,8,9. By binding to specific sequences10, CTCF defines contact points for cohesin-mediated long-range chromosomal cis-interactions1,2,4,5,6,7,11. Cohesin is also present at these sites12,13, but has been proposed to be loaded onto DNA elsewhere14,15 and to extrude chromatin loops until it encounters CTCF bound to DNA16,17,18,19. How cohesin is recruited to CTCF sites, according to this or other models, is unknown. Here we show that the distribution of cohesin in the mouse genome depends on transcription, CTCF and the cohesin release factor Wings apart-like (Wapl). In CTCF-depleted fibroblasts, cohesin cannot be properly recruited to CTCF sites but instead accumulates at transcription start sites of active genes, where the cohesin-loading complex is located14,15. In the absence of both CTCF and Wapl, cohesin accumulates in up to 70 kilobase-long regions at 3{${'}$}-ends of active genes, in particular if these converge on each other. Changing gene expression modulates the position of these `cohesin islands'. These findings indicate that transcription can relocate mammalian cohesin over long distances on DNA, as previously reported for yeast cohesin20,21,22,23, that this translocation contributes to positioning cohesin at CTCF sites, and that active genes can be freed from cohesin either by transcription-mediated translocation or by Wapl-mediated release.},
  language = {en},
  number = {7651},
  journal = {Nature},
  doi = {10.1038/nature22063},
  author = {Busslinger, Georg A. and Stocsits, Roman R. and van der Lelij, Petra and Axelsson, Elin and Tedeschi, Antonio and Galjart, Niels and Peters, Jan-Michael},
  month = apr,
  year = {2017},
  pages = {503-507},
  file = {/home/bbeltr1/Documents/paper-collection/PetersJ/Busslinger et al_2017_Cohesin is positioned in mammalian genomes by transcription, CTCF and Wapl.pdf;/home/bbeltr1/Documents/zotero/storage/VFUXPY35/nature22063.html}
}

@article{stigler2016,
  title = {Single-{{Molecule Imaging Reveals}} a {{Collapsed Conformational State}} for {{DNA}}-{{Bound Cohesin}}},
  volume = {15},
  issn = {2211-1247},
  abstract = {Summary
Cohesin is essential for the hierarchical organization of the eukaryotic genome and plays key roles in many aspects of chromosome biology. The conformation of cohesin bound to DNA remains poorly defined, leaving crucial gaps in our understanding of how cohesin fulfills its biological functions. Here, we use single-molecule microscopy to directly observe the dynamic and functional characteristics of cohesin bound to DNA. We show that cohesin can undergo rapid one-dimensional (1D) diffusion along DNA, but individual nucleosomes, nucleosome arrays, and other protein obstacles significantly restrict its mobility. Furthermore, we demonstrate that DNA motor proteins can readily push cohesin along DNA, but they cannot pass through the interior of the cohesin ring. Together, our results reveal that DNA-bound cohesin has a central pore that is substantially smaller than anticipated. These findings have direct implications for understanding how cohesin and other SMC proteins interact with and distribute along chromatin.},
  number = {5},
  journal = {Cell Reports},
  doi = {10.1016/j.celrep.2016.04.003},
  author = {Stigler, Johannes and {\c C}amdere, Gamze \"O. and Koshland, Douglas E. and Greene, Eric C.},
  month = may,
  year = {2016},
  pages = {988-998},
  file = {/home/bbeltr1/Documents/paper-collection/GreeneE/Stigler et al_2016_Single-Molecule Imaging Reveals a Collapsed Conformational State for DNA-Bound.pdf;/home/bbeltr1/Documents/zotero/storage/LSQIZ5AH/S2211124716304028.html}
}

@article{kanke2016,
  title = {Cohesin Acetylation and {{Wapl}}-{{Pds5}} Oppositely Regulate Translocation of Cohesin along {{DNA}}},
  volume = {35},
  copyright = {\textcopyright{} 2016 The Authors},
  issn = {0261-4189, 1460-2075},
  abstract = {Cohesin is a ring-shaped protein complex that plays a crucial role in sister chromatid cohesion and gene expression. The dynamic association of cohesin with chromatin is essential for these functions. However, the exact nature of cohesin dynamics, particularly cohesin translocation, remains unclear. We evaluated the dynamics of individual cohesin molecules on DNA and found that the cohesin core complex possesses an intrinsic ability to traverse DNA in an adenosine triphosphatase (ATPase)-dependent manner. Translocation ability is suppressed in the presence of Wapl-Pds5 and Sororin; this suppression is alleviated by the acetylation of cohesin and the action of mitotic kinases. In Xenopus laevis egg extracts, cohesin is translocated on unreplicated DNA in an ATPase- and Smc3 acetylation-dependent manner. Cohesin movement changes from bidirectional to unidirectional when cohesin faces DNA replication; otherwise, it is incorporated into replicating DNA without being translocated or is dissociated from replicating DNA. This study provides insight into the nature of individual cohesin dynamics and the mechanisms by which cohesin achieves cohesion in different chromatin contexts.
Synopsis

{$<$}img class="highwire-embed" alt="Embedded Image" src="http://emboj.embopress.org.stanford.idm.oclc.org/sites/default/files/highwire/embojnl/35/24/2686/embed/graphic-1.gif"/{$>$}

Single-molecule observations of individual cohesin rings on DNA define how regulatory factors such as acetylation, Wapl-Pds5, and Sororin, as well as DNA replication influence cohesin translocation in vitro and in Xenopus egg extracts.

Scc2-Scc4-dependent topological loading of cohesin is required for cohesin translocation along DNA.Acetylation of cohesin by Esco1 (or Xenopus XEco2) promotes cohesin translocation along DNA and chromatin.Cohesin translocation is suppressed by Wapl-Pds5 and Sororin, and facilitated by Aurora B-mediated phosphorylation.Cohesin is preferentially present and translocated in nucleosome-poor region of unreplicated chromatin.Upon DNA replication, cohesin is either (i) stalled and incorporated into replicating DNA, (ii) translocated with replication, or (iii) dissociated from replicating DNA.},
  language = {en},
  number = {24},
  journal = {The EMBO Journal},
  doi = {10.15252/embj.201695756},
  author = {Kanke, Mai and Tahara, Eri and in't Veld, Pim J. Huis and Nishiyama, Tomoko},
  month = dec,
  year = {2016},
  keywords = {DNA replication,chromosome segregation,cohesin,post‐translational modification,single‐molecule TIRF microscopy},
  pages = {2686-2698},
  file = {/home/bbeltr1/Documents/paper-collection/NishiyamaT/Kanke et al_2016_Cohesin acetylation and Wapl‐Pds5 oppositely regulate translocation of cohesin.pdf;/home/bbeltr1/Documents/zotero/storage/CCM3QLSI/2686.html},
  pmid = {27872142}
}

@article{davidson2016,
  title = {Rapid Movement and Transcriptional Re-Localization of Human Cohesin on {{DNA}}},
  volume = {35},
  copyright = {\textcopyright{} 2016 The Authors. Published under the terms of the CC BY 4.0 license},
  issn = {1460-2075},
  abstract = {The spatial organization, correct expression, repair, and segregation of eukaryotic genomes depend on cohesin, ring-shaped protein complexes that are thought to function by entrapping DNA. It has been proposed that cohesin is recruited to specific genomic locations from distal loading sites by an unknown mechanism, which depends on transcription, and it has been speculated that cohesin movements along DNA could create three-dimensional genomic organization by loop extrusion. However, whether cohesin can translocate along DNA is unknown. Here, we used single-molecule imaging to show that cohesin can diffuse rapidly on DNA in a manner consistent with topological entrapment and can pass over some DNA-bound proteins and nucleosomes but is constrained in its movement by transcription and DNA-bound CCCTC-binding factor (CTCF). These results indicate that cohesin can be positioned in the genome by moving along DNA, that transcription can provide directionality to these movements, that CTCF functions as a boundary element for moving cohesin, and they are consistent with the hypothesis that cohesin spatially organizes the genome via loop extrusion.},
  language = {en},
  number = {24},
  journal = {The EMBO Journal},
  doi = {10.15252/embj.201695402},
  author = {Davidson, Iain F. and Goetz, Daniela and Zaczek, Maciej P. and Molodtsov, Maxim I. and in 't Veld, Pim J. Huis and Weissmann, Florian and Litos, Gabriele and Cisneros, David A. and Ocampo-Hafalla, Maria and Ladurner, Rene and Uhlmann, Frank and Vaziri, Alipasha and Peters, Jan-Michael},
  month = oct,
  year = {2016},
  keywords = {transcription,cohesin,cell cycle,genome organization,single-molecule TIRF microscopy},
  pages = {2671-2685},
  file = {/home/bbeltr1/Documents/paper-collection/PetersJ/Davidson et al_2016_Rapid movement and transcriptional re-localization of human cohesin on DNA.pdf;/home/bbeltr1/Documents/zotero/storage/6ICHGHES/embj.html}
}

@article{sofueva2013,
  title = {Cohesin-mediated Interactions Organize Chromosomal Domain Architecture},
  volume = {32},
  copyright = {Copyright \textcopyright{} 2013 European Molecular Biology Organization. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.},
  issn = {0261-4189, 1460-2075},
  abstract = {To ensure proper gene regulation within constrained nuclear space, chromosomes facilitate access to transcribed regions, while compactly packaging all other information. Recent studies revealed that chromosomes are organized into megabase-scale domains that demarcate active and inactive genetic elements, suggesting that compartmentalization is important for genome function. Here, we show that very specific long-range interactions are anchored by cohesin/CTCF sites, but not cohesin-only or CTCF-only sites, to form a hierarchy of chromosomal loops. These loops demarcate topological domains and form intricate internal structures within them. Post-mitotic nuclei deficient for functional cohesin exhibit global architectural changes associated with loss of cohesin/CTCF contacts and relaxation of topological domains. Transcriptional analysis shows that this cohesin-dependent perturbation of domain organization leads to widespread gene deregulation of both cohesin-bound and non-bound genes. Our data thereby support a role for cohesin in the global organization of domain structure and suggest that domains function to stabilize the transcriptional programmes within them.
There is a Have you seen? (December 2013) associated with this Article.},
  language = {en},
  number = {24},
  journal = {The EMBO Journal},
  doi = {10.1038/emboj.2013.237},
  author = {Sofueva, Sevil and Yaffe, Eitan and Chan, Wen-Ching and Georgopoulou, Dimitra and Rudan, Matteo Vietri and Mira-Bontenbal, Hegias and Pollard, Steven M. and Schroth, Gary P. and Tanay, Amos and Hadjur, Suzana},
  month = dec,
  year = {2013},
  keywords = {transcription,chromosome organization,cohesin},
  pages = {3119-3129},
  file = {/home/bbeltr1/Documents/paper-collection/HadjurS/Sofueva et al_2013_Cohesin‐mediated interactions organize chromosomal domain architecture.pdf;/home/bbeltr1/Documents/zotero/storage/VRHUHFI6/3119.html},
  pmid = {24185899}
}

@article{zuin2014,
  title = {Cohesin and {{CTCF}} Differentially Affect Chromatin Architecture and Gene Expression in Human Cells},
  volume = {111},
  issn = {0027-8424, 1091-6490},
  abstract = {Recent studies of genome-wide chromatin interactions have revealed that the human genome is partitioned into many self-associating topological domains. The boundary sequences between domains are enriched for binding sites of CTCC-binding factor (CTCF) and the cohesin complex, implicating these two factors in the establishment or maintenance of topological domains. To determine the role of cohesin and CTCF in higher-order chromatin architecture in human cells, we depleted the cohesin complex or CTCF and examined the consequences of loss of these factors on higher-order chromatin organization, as well as the transcriptome. We observed a general loss of local chromatin interactions upon disruption of cohesin, but the topological domains remain intact. However, we found that depletion of CTCF not only reduced intradomain interactions but also increased interdomain interactions. Furthermore, distinct groups of genes become misregulated upon depletion of cohesin and CTCF. Taken together, these observations suggest that CTCF and cohesin contribute differentially to chromatin organization and gene regulation.},
  language = {en},
  number = {3},
  journal = {PNAS},
  doi = {10.1073/pnas.1317788111},
  author = {Zuin, Jessica and Dixon, Jesse R. and van der Reijden, Michael I. J. A. and Ye, Zhen and Kolovos, Petros and Brouwer, Rutger W. W. and van de Corput, Mari\"ette P. C. and van de Werken, Harmen J. G. and Knoch, Tobias A. and van IJcken, Wilfred F. J. and Grosveld, Frank G. and Ren, Bing and Wendt, Kerstin S.},
  month = jan,
  year = {2014},
  keywords = {Hi-C,4C,HOX cluster,transcriptional regulation},
  pages = {996-1001},
  file = {/home/bbeltr1/Documents/paper-collection/WendtK/Zuin et al_2014_Cohesin and CTCF differentially affect chromatin architecture and gene.pdf;/home/bbeltr1/Documents/zotero/storage/Z56WGYA8/996.html},
  pmid = {24335803}
}

@article{seitan2013,
  title = {Cohesin-Based Chromatin Interactions Enable Regulated Gene Expression within Preexisting Architectural Compartments},
  volume = {23},
  issn = {1088-9051, 1549-5469},
  abstract = {Chromosome conformation capture approaches have shown that interphase chromatin is partitioned into spatially segregated Mb-sized compartments and sub-Mb-sized topological domains. This compartmentalization is thought to facilitate the matching of genes and regulatory elements, but its precise function and mechanistic basis remain unknown. Cohesin controls chromosome topology to enable DNA repair and chromosome segregation in cycling cells. In addition, cohesin associates with active enhancers and promoters and with CTCF to form long-range interactions important for gene regulation. Although these findings suggest an important role for cohesin in genome organization, this role has not been assessed on a global scale. Unexpectedly, we find that architectural compartments are maintained in noncycling mouse thymocytes after genetic depletion of cohesin in vivo. Cohesin was, however, required for specific long-range interactions within compartments where cohesin-regulated genes reside. Cohesin depletion diminished interactions between cohesin-bound sites, whereas alternative interactions between chromatin features associated with transcriptional activation and repression became more prominent, with corresponding changes in gene expression. Our findings indicate that cohesin-mediated long-range interactions facilitate discrete gene expression states within preexisting chromosomal compartments.},
  language = {en},
  number = {12},
  journal = {Genome Res.},
  doi = {10.1101/gr.161620.113},
  author = {Seitan, Vlad C. and Faure, Andre J. and Zhan, Ye and McCord, Rachel Patton and Lajoie, Bryan R. and {Ing-Simmons}, Elizabeth and Lenhard, Boris and Giorgetti, Luca and Heard, Edith and Fisher, Amanda G. and Flicek, Paul and Dekker, Job and Merkenschlager, Matthias},
  month = jan,
  year = {2013},
  pages = {2066-2077},
  file = {/home/bbeltr1/Documents/paper-collection/MerkenschlagerM/Seitan et al_2013_Cohesin-based chromatin interactions enable regulated gene expression within.pdf;/home/bbeltr1/Documents/zotero/storage/GVC8RHEY/2066.html},
  pmid = {24002784}
}

@article{tedeschi2013,
  title = {Wapl Is an Essential Regulator of Chromatin Structure and Chromosome Segregation},
  volume = {501},
  copyright = {2013 Nature Publishing Group},
  issn = {1476-4687},
  abstract = {Mammalian genomes contain several billion base pairs of DNA that are packaged in chromatin fibres. At selected gene loci, cohesin complexes have been proposed to arrange these fibres into higher-order structures1,2,3,4,5,6,7, but how important this function is for determining overall chromosome architecture and how the process is regulated are not well understood. Using conditional mutagenesis in the mouse, here we show that depletion of the cohesin-associated protein Wapl8,9 stably locks cohesin on DNA, leads to clustering of cohesin in axial structures, and causes chromatin condensation in interphase chromosomes. These findings reveal that the stability of cohesin\textendash{}DNA interactions is an important determinant of chromatin structure, and indicate that cohesin has an architectural role in interphase chromosome territories. Furthermore, we show that regulation of cohesin\textendash{}DNA interactions by Wapl is important for embryonic development, expression of genes such as c-myc (also known as Myc), and cell cycle progression. In mitosis, Wapl-mediated release of cohesin from DNA is essential for proper chromosome segregation and protects cohesin from cleavage by the protease separase, thus enabling mitotic exit in the presence of functional cohesin complexes.},
  language = {en},
  number = {7468},
  journal = {Nature},
  doi = {10.1038/nature12471},
  author = {Tedeschi, Antonio and Wutz, Gordana and Huet, S\'ebastien and Jaritz, Markus and Wuensche, Annelie and Schirghuber, Erika and Davidson, Iain Finley and Tang, Wen and Cisneros, David A. and Bhaskara, Venugopal and Nishiyama, Tomoko and Vaziri, Alipasha and Wutz, Anton and Ellenberg, Jan and Peters, Jan-Michael},
  month = sep,
  year = {2013},
  pages = {564-568},
  file = {/home/bbeltr1/Documents/paper-collection/PetersJ/Tedeschi et al_2013_Wapl is an essential regulator of chromatin structure and chromosome segregation.pdf;/home/bbeltr1/Documents/zotero/storage/HF8NC2EB/nature12471.html}
}

@article{hansen2018,
  title = {Recent Evidence That {{TADs}} and Chromatin Loops Are Dynamic Structures},
  volume = {9},
  issn = {1949-1034, 1949-1042},
  abstract = {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 ringshaped 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.},
  language = {en},
  number = {1},
  journal = {Nucleus},
  doi = {10.1080/19491034.2017.1389365},
  author = {Hansen, Anders S. and Cattoglio, Claudia and Darzacq, Xavier and Tjian, Robert},
  month = jan,
  year = {2018},
  pages = {20-32},
  file = {/home/bbeltr1/Documents/paper-collection/TjianR/Hansen et al_2018_Recent evidence that TADs and chromatin loops are dynamic structures.pdf}
}

@article{wutz2017,
  title = {Topologically Associating Domains and Chromatin Loops Depend on Cohesin and Are Regulated by {{CTCF}}, {{WAPL}}, and {{PDS5}} Proteins},
  volume = {36},
  copyright = {\textcopyright{} 2017 The Authors},
  issn = {1460-2075},
  abstract = {Mammalian genomes are spatially organized into compartments, topologically associating domains (TADs), and loops to facilitate gene regulation and other chromosomal functions. How compartments, TADs, and loops are generated is unknown. It has been proposed that cohesin forms TADs and loops by extruding chromatin loops until it encounters CTCF, but direct evidence for this hypothesis is missing. Here, we show that cohesin suppresses compartments but is required for TADs and loops, that CTCF defines their boundaries, and that the cohesin unloading factor WAPL and its PDS5 binding partners control the length of loops. In the absence of WAPL and PDS5 proteins, cohesin forms extended loops, presumably by passing CTCF sites, accumulates in axial chromosomal positions (vermicelli), and condenses chromosomes. Unexpectedly, PDS5 proteins are also required for boundary function. These results show that cohesin has an essential genome-wide function in mediating long-range chromatin interactions and support the hypothesis that cohesin creates these by loop extrusion, until it is delayed by CTCF in a manner dependent on PDS5 proteins, or until it is released from DNA by WAPL.},
  language = {en},
  number = {24},
  journal = {The EMBO Journal},
  doi = {10.15252/embj.201798004},
  author = {Wutz, Gordana and V\'arnai, Csilla and Nagasaka, Kota and Cisneros, David A. and Stocsits, Roman R. and Tang, Wen and Schoenfelder, Stefan and Jessberger, Gregor and Muhar, Matthias and Hossain, M. Julius and Walther, Nike and Koch, Birgit and Kueblbeck, Moritz and Ellenberg, Jan and Zuber, Johannes and Fraser, Peter and Peters, Jan-Michael},
  year = {2017},
  keywords = {chromatin structure,genome organization,chromatin condensation,loop extrusion,vermicelli},
  pages = {3573-3599},
  file = {/home/bbeltr1/Documents/paper-collection/PetersJ/Wutz et al_2017_Topologically associating domains and chromatin loops depend on cohesin and are.pdf;/home/bbeltr1/Documents/zotero/storage/IJD6Z7DJ/embj.html}
}

@article{ruiz-velasco2017,
  series = {Future of {{Systems Biology}} \textbullet{} {{Genomics}} and Epigenomics},
  title = {Structure Meets Function: {{How}} Chromatin Organisation Conveys Functionality},
  volume = {1},
  issn = {2452-3100},
  shorttitle = {Structure Meets Function},
  abstract = {Understanding how the genome is compacted in a highly ordered structure that fits in the eukaryotic nucleus, while keeping its capacity of orchestrating the functionality of the cell, is one of the long-standing questions in biology. While the recent technological advances in chromosome conformation capture experiments have provided extensive knowledge about the structural organisation of chromatin, our understanding of the functional impact of these arrangements on downstream processes, and how structure translates into function, is just beginning to emerge. In this review we summarize our current knowledge of the three-dimensional chromatin organisation, the mechanisms of how it is established and maintained, and the functional impact it has on gene regulation and complex phenotypes. We will end with a discussion on the future developments of this fast-paced field.},
  journal = {Current Opinion in Systems Biology},
  doi = {10.1016/j.coisb.2017.01.003},
  author = {{Ruiz-Velasco}, Mariana and Zaugg, Judith B.},
  month = feb,
  year = {2017},
  pages = {129-136},
  file = {/home/bbeltr1/Documents/paper-collection/ZauggJ/Ruiz-Velasco_Zaugg_2017_Structure meets function.pdf;/home/bbeltr1/Documents/zotero/storage/FCJ5YGDL/S2452310017300173.html}
}

@article{dekker2016,
  title = {The {{3D Genome}} as {{Moderator}} of {{Chromosomal Communication}}},
  volume = {164},
  issn = {0092-8674, 1097-4172},
  language = {English},
  number = {6},
  journal = {Cell},
  doi = {10.1016/j.cell.2016.02.007},
  author = {Dekker, Job and Mirny, Leonid},
  month = mar,
  year = {2016},
  keywords = {gene regulation,CTCF,Hi-C,cohesin,biophysics,condensin,domains,enhancer,gene expression,polymers,promoter,simulations},
  pages = {1110-1121},
  file = {/home/bbeltr1/Documents/paper-collection/MirnyL/Dekker_Mirny_2016_The 3D Genome as Moderator of Chromosomal Communication.pdf;/home/bbeltr1/Documents/zotero/storage/BGWZ4Z2H/S0092-8674(16)30073-3.html},
  pmid = {26967279}
}

@article{jun2003,
  title = {Diffusion-Limited Loop Formation of Semiflexible Polymers: {{Kramers}} Theory and the Intertwined Time Scales of Chain Relaxation and Closing},
  volume = {64},
  issn = {0295-5075, 1286-4854},
  shorttitle = {Diffusion-Limited Loop Formation of Semiflexible Polymers},
  abstract = {We show that Kramers rate theory gives a straightforward, accurate estimate of the closing time {$\tau$}c of a semiflexible polymer that is valid in cases of physical interest. The calculation also reveals how the time scales of chain relaxation and closing are intertwined, illuminating an apparent conflict between two ways of calculating {$\tau$}c in the flexible limit.},
  language = {en},
  number = {3},
  journal = {Europhysics Letters (EPL)},
  doi = {10.1209/epl/i2003-00219-7},
  author = {Jun, S and Bechhoefer, J and Ha, B.-Y},
  month = nov,
  year = {2003},
  pages = {420-426},
  file = {/home/bbeltr1/Documents/paper-collection/HaB/Jun et al_2003_Diffusion-limited loop formation of semiflexible polymers.pdf}
}

@article{guerin2013,
  archivePrefix = {arXiv},
  eprinttype = {arxiv},
  eprint = {1211.4700},
  title = {Reactive Conformations and Non-{{Markovian}} Cyclization Kinetics of a {{Rouse}} Polymer},
  volume = {138},
  issn = {0021-9606, 1089-7690},
  abstract = {We investigate theoretically the physics of diffusion-limited intramolecular polymer reactions. The present work completes and goes beyond a previous study [Nat. Chem. 4, 268 (2012)] that showed that the distribution of the polymer conformations at the very instant of reaction plays a key role in the cyclization kinetics, and takes explicitly into account the non-Markovian nature of the reactant motion. Here, we present in detail this non-Markovian theory, and compare it explicitly with existing Markovian theories and with numerical stochastic simulations. A large focus is made on the description of the non-equilibrium reactive conformations, with both numerical and analytical tools. We show that the reactive conformations are elongated and are characterized by a spectrum with a slowly decreasing tail, implying that the monomers that neighbor the reactive monomers are significantly shifted at the instant of reaction. We complete the study by deriving explicit formulas for the reaction rates in the Markovian Wilemski-Fixman theory when the reactants are located in arbitrary positions in the chain. We also give a simple scaling argument to understand the existence of two regimes in the reaction time, that come from two possible behaviors of monomer motion which can be either diffusive or subdiffusive.},
  language = {en},
  number = {9},
  journal = {The Journal of Chemical Physics},
  doi = {10.1063/1.4792437},
  author = {Gu\'erin, T. and B\'enichou, O. and Voituriez, R.},
  month = mar,
  year = {2013},
  keywords = {Condensed Matter - Soft Condensed Matter,Condensed Matter - Statistical Mechanics,Physics - Chemical Physics},
  pages = {094908},
  file = {/home/bbeltr

license: MIT

license_type: permissive

branch_name: refs/heads/master

extension: bib