Models for chromatin remodeling: a critical comparison

2003 ◽  
Vol 81 (3) ◽  
pp. 169-172 ◽  
Author(s):  
K van Holde ◽  
T Yager
Keyword(s):  
Diffusion Model ◽  
Chromatin Remodeling ◽  
Experimental Studies ◽  
Nucleosome Remodeling ◽  
Defect Generation ◽  
Critical Comparison ◽  
Nucleosomal Dna ◽  
Reptation Model ◽  
Cast Doubt ◽  
Random Diffusion

Nucleosome remodeling has been shown, in many cases, to involve cis displacement of nucleosomes on the DNA. This process seems similar to the long-recognized random diffusion of nucleosomes along DNA, but the remodeling process is unidirectional and ATP dependent. Several years ago, we developed a model for nucleosome migration, based on the diffusion of "twist-defects" within the nucleosomal DNA. This has been modified into a model that incorporates ATP-dependent defect generation, and can account for many observations concerning remodeling. However, certain experimental studies in recent years have cast doubt on the applicability of the twist-diffusion model for remodeling, and seem to favor instead a "reptation" model. We discuss herein these problems and propose a resolution.Key words: nucleosome, remodeling, chromatin.

scholarly journals Dependency of ISW1a Chromatin Remodeling on Extranucleosomal DNA

2007 ◽  
Vol 27 (8) ◽  
pp. 3217-3225 ◽  
Author(s):  
Vamsi K. Gangaraju ◽  
Blaine Bartholomew
Keyword(s):  
Atpase Activity ◽  
Chromatin Remodeling ◽  
Molecular Basis ◽  
The Other ◽  
Entry And Exit ◽  
Exit Site ◽  
Optimal Length ◽  
Nucleosome Remodeling ◽  
Dna Footprinting ◽  
Nucleosomal Dna

ABSTRACT The nucleosome remodeling activity of ISW1a was dependent on whether ISW1a was bound to one or both extranucleosomal DNAs. ISW1a preferentially bound nucleosomes with an optimal length of ∼33 to 35 bp of extranucleosomal DNA at both the entry and exit sites over nucleosomes with extranucleosomal DNA at only one entry or exit site. Nucleosomes with extranucleosomal DNA at one of the entry/exit sites were readily remodeled by ISW1a and stimulated the ATPase activity of ISW1a, while conversely, nucleosomes with extranucleosomal DNA at both entry/exit sites were unable either to stimulate the ATPase activity of ISW1a or to be mobilized. DNA footprinting revealed that a major conformational difference between the nucleosomes was the lack of ISW1a binding to nucleosomal DNA two helical turns from the dyad axis in nucleosomes with extranucleosomal DNA at both entry/exit sites. The Ioc3 subunit of ISW1a was found to be the predominant subunit associated with extranucleosomal DNA when ISW1a is bound either to one or to both extranucleosomal DNAs. These two conformations of the ISW1a-nucleosome complex are suggested to be the molecular basis for the nucleosome spacing activity of ISW1a on nucleosomal arrays. ISW1b, the other isoform of ISW1, does not have the same dependency for extranucleosomal DNA as ISW1a and, likewise, is not able to space nucleosomes.

scholarly journals Structure of the primed state of the ATPase domain of chromatin remodeling factor ISWI bound to the nucleosome

2019 ◽  
Vol 47 (17) ◽  
pp. 9400-9409 ◽  
Author(s):  
Sagar Chittori ◽  
Jingjun Hong ◽  
Yawen Bai ◽  
Sriram Subramaniam
Keyword(s):  
Electron Microscopy ◽  
Chromatin Remodeling ◽  
Initial Step ◽  
Atpase Domain ◽  
Nucleosome Remodeling ◽  
Cryo Electron Microscopy ◽  
Nucleosomal Dna ◽  
Primed State ◽  
Histone Core

Abstract ATP-dependent chromatin remodeling factors of SWI/SNF2 family including ISWI, SNF2, CHD1 and INO80 subfamilies share a conserved but functionally non-interchangeable ATPase domain. Here we report cryo-electron microscopy (cryo-EM) structures of the nucleosome bound to an ISWI fragment with deletion of the AutoN and HSS regions in nucleotide-free conditions and the free nucleosome at ∼ 4 Å resolution. In the bound conformation, the ATPase domain interacts with the super helical location 2 (SHL 2) of the nucleosomal DNA, with the N-terminal tail of H4 and with the α1 helix of H3. Density for other regions of ISWI is not observed, presumably due to disorder. Comparison with the structure of the free nucleosome reveals that although the histone core remains largely unchanged, remodeler binding causes perturbations in the nucleosomal DNA resulting in a bulge near the SHL2 site. Overall, the structure of the nucleotide-free ISWI-nucleosome complex is similar to the corresponding regions of the recently reported ADP bound ISWI-nucleosome structures, which are significantly different from that observed for the ADP-BeFx bound structure. Our findings are relevant to the initial step of ISWI binding to the nucleosome and provide additional insights into the nucleosome remodeling process driven by ISWI.

scholarly journals The SWI/SNF Complex Creates Loop Domains in DNA and Polynucleosome Arrays and Can Disrupt DNA-Histone Contacts within These Domains

1999 ◽  
Vol 19 (2) ◽  
pp. 1470-1478 ◽  
Author(s):  
David P. Bazett-Jones ◽  
Jacques Côté ◽  
Carolyn C. Landel ◽  
Craig L. Peterson ◽  
Jerry L. Workman
Keyword(s):  
Chromatin Remodeling ◽  
Dna Content ◽  
Naked Dna ◽  
Nucleosome Organization ◽  
Nucleosomal Dna ◽  
Close Proximity ◽  
Loop Domains

ABSTRACT To understand the mechanisms by which the chromatin-remodeling SWI/SNF complex interacts with DNA and alters nucleosome organization, we have imaged the SWI/SNF complex with both naked DNA and nucleosomal arrays by using energy-filtered microscopy. By making ATP-independent contacts with DNA at multiple sites on its surface, SWI/SNF creates loops, bringing otherwise-distant sites into close proximity. In the presence of ATP, SWI/SNF action leads to the disruption of nucleosomes within domains that appear to be topologically constrained by the complex. The data indicate that the action of one SWI/SNF complex on an array of nucleosomes can lead to the formation of a region where multiple nucleosomes are disrupted. Importantly, nucleosome disruption by SWI/SNF results in a loss of DNA content from the nucleosomes. This indicates a mechanism by which SWI/SNF unwraps part of the nucleosomal DNA.

scholarly journals Random diffusion model with structure corrections

2010 ◽  
Vol 81 (5) ◽  
Author(s):  
David D. McCowan ◽  
Gene F. Mazenko
Keyword(s):  
Diffusion Model ◽  
Random Diffusion

Dynamic epistasis analysis reveals how chromatin remodeling regulates transcriptional bursting

2021 ◽  
Author(s):  
Ineke Brouwer ◽  
Emma Kerklingh ◽  
Fred van Leeuwen ◽  
Tineke L Lenstra
Keyword(s):  
Transcription Factor ◽  
Chromatin Remodeling ◽  
Single Molecule ◽  
Binding Sites ◽  
Live Cell Imaging ◽  
Cell Imaging ◽  
Nucleosome Remodeling ◽  
Epistasis Analysis ◽  
Transcriptional Bursting ◽  
Kinetics Of

Transcriptional bursting has been linked to the stochastic positioning of nucleosomes. However, how bursting is regulated by remodeling of promoter nucleosomes is unknown. Here, we use single-molecule live-cell imaging of GAL10 transcription in budding yeast to measure how transcriptional bursting changes upon single and double perturbations of chromatin remodeling factors, the transcription factor Gal4 and preinitiation complex (PIC) components. Using dynamic epistasis analysis, we reveal how remodeling of different nucleosomes regulates individual transcriptional bursting parameters. At the nucleosome covering the Gal4 binding sites, RSC acts synergistically with Gal4 binding to facilitate each burst. Conversely, nucleosome remodeling at the TATA box controls only the first burst upon galactose induction. In the absence of remodelers, nucleosomes at canonical TATA boxes are displaced by TBP binding to allow for transcription activation. Overall, our results reveal how promoter nucleosome remodeling, together with transcription factor and PIC binding regulates the kinetics of transcriptional bursting.

Friction Induced Brake Vibrations at Low Speeds: Experiments, State-Space Reconstruction and Implications on Modeling

2006 ◽  
Author(s):  
Hartmut Hetzler ◽  
Wolfgang Seemann
Keyword(s):  
Classical Model ◽  
A Priori ◽  
Experimental Studies ◽  
Low Frequency ◽  
Disc Brake ◽  
Minimal Models ◽  
Stick Slip ◽  
Cast Doubt ◽  
Vibration Pattern ◽  
Embedding Methods

Today, low frequency disc-brake noises are commonly explained as self-sustained stick-slip oscillations. Although, at a first glance this explanation seems reasonable, there are indices that cast doubt on it. For instance, the basic frequency of the observed oscillations does not scale with the disc-speed as it is with stick-slip oscillations and the classical model does not explain the observed ending of the vibrations beyond a certain speed. Indeed, our experimental studies on groaning noises reveal two different vibration patterns: stick-slip vibrations at almost vanishing relative speed and a second, differing vibration pattern at low to moderate relative speeds. Yet, these two patterns produce a very similar acoustic impression. While the experiment provides a vast amount of data, the dimension and structure of the underlying oscillation is not known a priori – hence, constructing phenomenological minimal models usually must rely on assumptions, e.g. about the number of DOF, etc. Due to noise and complexity, the measured raw data did only allow for a first straight forward insight, rendering further analysis necessary. Hence, time-delay embedding methods together with a principle component analysis were used to reconstruct a pseudo-phase space together with the embedded attractor to analyse for the system's dimension and to separate signal from noise.

Further analytical and experimental studies on the shoot apex of Helianthus annuus: variable activity in the central zone

1979 ◽  
Vol 57 (8) ◽  
pp. 971-980 ◽  
Author(s):  
E. L. Davis ◽  
Patricia Rennie ◽  
Taylor A. Steeves
Keyword(s):  
Helianthus Annuus ◽  
Mitotic Activity ◽  
Shoot Apex ◽  
Experimental Studies ◽  
Central Zone ◽  
Peripheral Zone ◽  
Intact Plants ◽  
Cast Doubt ◽  
Young Leaves ◽  
Mitotic Frequency

The cytologically distinctive central zone of the vegetative shoot apex of Helianthus annuus L. cv. Peredovic has a mitotic frequency considerably lower than that of the surrounding peripheral zone in intact plants. Apices excised and grown in culture for 5 days before being supplied with [H3]thymidine reveal a correspondingly low level of DNA synthesis in the central zone when autoradiographed. In similarly cultured apices, mitotic activity in the central zone is less than that recorded for intact plants. Labelling immediately after excision of the apex indicates that the central zone cells are activated by the operation and quiescence returns during the following 5 days. This activation is confirmed by mitotic counts 2 days after excision. The removal of only two young leaves from the apical buds of otherwise intact plants results in a comparable stimulation of mitotic activity in the central zone. These observations cast doubt upon the significance of mitotic activity in living shoot apices when these have been exposed for observation by removal of leaves. They also raise questions about the validity of labelling techniques which involve the partial dissection of the shoot apex.

scholarly journals RSC2, Encoding a Component of the RSC Nucleosome Remodeling Complex, Is Essential for 2μm Plasmid Maintenance in Saccharomyces cerevisiae

2002 ◽  
Vol 22 (12) ◽  
pp. 4218-4229 ◽  
Author(s):  
Michael C. V. L. Wong ◽  
Suzanna R. S. Scott-Drew ◽  
Matthew J. Hayes ◽  
Philip J. Howard ◽  
James A. H. Murray
Keyword(s):  
Chromatin Remodeling ◽  
Chromatin Structure ◽  
Plasmid Dna ◽  
Direct Evidence ◽  
Maternal Inheritance ◽  
Alternative Form ◽  
Nucleosome Remodeling ◽  
Daughter Cells ◽  
Chromatin Remodeling Complex ◽  
Stable Maintenance

ABSTRACT The stable maintenance of the 2μm circle plasmid depends on its ability to overcome intrinsic maternal inheritance bias, which in yeast normally results in the failure to transmit DNA molecules efficiently to daughter cells. In addition to the plasmid proteins Rep1 and Rep2 acting on the plasmid DNA locus STB, it is likely that other chromosomally encoded yeast proteins are required. We have isolated mutants of yeast unable to maintain 2μm and found that RSC2 is essential for 2μm to overcome maternal inheritance bias. Rsc2 is part of a multisubunit RSC chromatin remodeling complex, and we show that in the absence of Rsc2 the chromatin structure of the STB region is significantly altered and the Rep1 protein loses its normal localization to subnuclear foci. Rsc1, a closely related homolog of Rsc2 present in an alternative form of the RSC complex, is not required for 2μm maintenance and does not replace the requirement for Rsc2 when overexpressed. This represents the first specific role for Rsc2 that has been related to a change in chromatin structure, as well as the first direct evidence linking chromatin structure to 2μm segregation.

scholarly journals The Roles of SNF2/SWI2 Nucleosome Remodeling Enzymes in Blood Cell Differentiation and Leukemia

2015 ◽  
Vol 2015 ◽  
pp. 1-17 ◽  
Author(s):  
Punit Prasad ◽  
Andreas Lennartsson ◽  
Karl Ekwall
Keyword(s):  
Blood Cell ◽  
Chromatin Remodeling ◽  
Large Scale ◽  
Cell Development ◽  
Normal Blood ◽  
Aberrant Expression ◽  
Atpase Subunit ◽  
Hematopoietic Stem ◽  
Nucleosome Remodeling ◽  
Genes Encoding

Here, we review the role of sucrose nonfermenting (SNF2) family enzymes in blood cell development. The SNF2 family comprises helicase-like ATPases, originally discovered in yeast, that can remodel chromatin by changing chromatin structure and composition. The human genome encodes 30 different SNF2 enzymes. SNF2 family enzymes are often part of multisubunit chromatin remodeling complexes (CRCs), which consist of noncatalytic/auxiliary subunit along with the ATPase subunit. However, blood cells express a limited set of SNF2 ATPases that are necessary to maintain the pool of hematopoietic stem cells (HSCs) and drive normal blood cell development and differentiation. The composition of CRCs can be altered by the association of specific auxiliary subunits. Several auxiliary CRC subunits have specific functions in hematopoiesis. Aberrant expressions of SNF2 ATPases and/or auxiliary CRC subunit(s) are often observed in hematological malignancies. Using large-scale data from the International Cancer Genome Consortium (ICGC) we observed frequent mutations in genes encoding SNF2 helicase-like enzymes and auxiliary CRC subunits in leukemia. Hence, orderly function of SNF2 family enzymes is crucial for the execution of normal blood cell developmental program, and defects in chromatin remodeling caused by mutations or aberrant expression of these proteins may contribute to leukemogenesis.

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