Relevant bibliographies by topics / Nucleosome in the cell

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Academic literature on the topic 'Nucleosome in the cell'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "Nucleosome in the cell"

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Zofall, Martin, Jim Persinger, and Blaine Bartholomew. "Functional Role of Extranucleosomal DNA and the Entry Site of the Nucleosome in Chromatin Remodeling by ISW2." Molecular and Cellular Biology 24, no. 22 (November 15, 2004): 10047–57. http://dx.doi.org/10.1128/mcb.24.22.10047-10057.2004.

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ABSTRACT A minimal amount of extranucleosomal DNA was required for nucleosome mobilization by ISW2 as shown by using a photochemical histone mapping approach to analyze nucleosome movement on a set of nucleosomes with varied lengths of extranucleosomal DNA. ISW2 was ineffective in repositioning or mobilizing nucleosomes with ≤20 bp of extranucleosomal DNA. In addition, ISW2 was able to slide nucleosomes to within only 10 to 13 bp of the edge of DNA fragments. The nucleosome mobilization was promoted by extranucleosomal single-stranded DNA with modest strand preference. Gaps (10 bp) just inside the nucleosome and in the extranucleosomal DNA showed that the transfer of torsional strain (twist) into the nucleosomal DNA region was not required for mobilizing nucleosomes. However, indications are that the extranucleosomal DNA immediately adjacent to the nucleosome has an important role in the initial stage of nucleosome movement by ISW2.
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Anderson, J. D., A. Thåström, and J. Widom. "Spontaneous Access of Proteins to Buried Nucleosomal DNA Target Sites Occurs via a Mechanism That Is Distinct from Nucleosome Translocation." Molecular and Cellular Biology 22, no. 20 (October 15, 2002): 7147–57. http://dx.doi.org/10.1128/mcb.22.20.7147-7157.2002.

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ABSTRACT Intrinsic nucleosome dynamics termed “site exposure” provides spontaneous and cooperative access to buried regions of nucleosomal DNA in vitro. Two different mechanisms for site exposure have been proposed, one based on nucleosome translocation, the other on dynamic nucleosome conformational changes in which a stretch of the nucleosomal DNA is transiently released off the histone surface. Here we report on three experiments that distinguish between these mechanisms. One experiment investigates the effects on the accessibilities of restriction enzyme target sites inside nucleosomes when extra DNA (onto which the nucleosome may move at low energetic cost) is appended onto one end. The other two experiments test directly for nucleosome mobility under the conditions used to probe accessibility to restriction enzymes: one on a selected nonnatural nucleosome positioning sequence, the other on the well-studied 5S rRNA gene nucleosome positioning sequence. We find from all three assays that restriction enzymes gain access to sites throughout the entire length of the nucleosomal DNA without contribution from nucleosome translocation. We conclude that site exposure in nucleosomes in vitro occurs via a nucleosome conformational change that leads to transient release of a stretch of DNA from the histone surface, most likely involving progressive uncoiling from an end. Recapture at a distal site along DNA that has partially uncoiled would result in looped structures which are believed to contribute to RNA polymerase elongation and may contribute to spontaneous or ATP-driven nucleosome mobility. Transient open states may facilitate the initial entry of transcription factors and enzymes in vivo.
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Feng, Jianxun, Haiyun Gan, Matthew L. Eaton, Hui Zhou, Shuqi Li, Jason A. Belsky, David M. MacAlpine, Zhiguo Zhang, and Qing Li. "Noncoding Transcription Is a Driving Force for Nucleosome Instability inspt16Mutant Cells." Molecular and Cellular Biology 36, no. 13 (May 2, 2016): 1856–67. http://dx.doi.org/10.1128/mcb.00152-16.

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FACT (facilitateschromatintranscription) consists of two essential subunits, Spt16 and Pob3, and functions as a histone chaperone. Mutation ofspt16results in a global loss of nucleosomes as well as aberrant transcription. Here, we show that the majority of nucleosome changes upon Spt16 depletion are alterations in nucleosome fuzziness and position shift. Most nucleosomal changes are suppressed by the inhibition of RNA polymerase II (Pol II) activity. Surprisingly, a small subgroup of nucleosome changes is resistant to transcriptional inhibition. Notably, Spt16 and distinct histone modifications are enriched at this subgroup of nucleosomes. We also report 1,037Spt16-suppressednoncodingtranscripts (SNTs) and found that the SNT start sites are enriched with the subgroup of nucleosomes resistant to Pol II inhibition. Finally, the nucleosomes at genes overlapping SNTs are more susceptible to changes upon Spt16 depletion than those without SNTs. Taken together, our results support a model in which Spt16 has a role in maintaining local nucleosome stability to inhibit initiation of SNT transcription, which once initiated drives additional nucleosome loss upon Spt16 depletion.
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Venturi, Christina Bourgeois, Alexander M. Erkine, and David S. Gross. "Cell Cycle-Dependent Binding of Yeast Heat Shock Factor to Nucleosomes." Molecular and Cellular Biology 20, no. 17 (September 1, 2000): 6435–48. http://dx.doi.org/10.1128/mcb.20.17.6435-6448.2000.

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ABSTRACT In the nucleus, transcription factors must contend with the presence of chromatin in order to gain access to their cognate regulatory sequences. As most nuclear DNA is assembled into nucleosomes, activators must either invade a stable, preassembled nucleosome or preempt the formation of nucleosomes on newly replicated DNA, which is transiently free of histones. We have investigated the mechanism by which heat shock factor (HSF) binds to target nucleosomal heat shock elements (HSEs), using as our model a dinucleosomal heat shock promoter (hsp82-ΔHSE1). We find that activated HSF cannot bind a stable, sequence-positioned nucleosome in G1-arrested cells. It can do so readily, however, following release from G1 arrest or after the imposition of either an early S- or late G2-phase arrest. Surprisingly, despite the S-phase requirement, HSF nucleosomal binding activity is restored in the absence of hsp82 replication. These results contrast with the prevailing paradigm for activator-nucleosome interactions and implicate a nonreplicative, S-phase-specific event as a prerequisite for HSF binding to nucleosomal sites in vivo.
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Kelbauskas, L., N. Woodbury, and D. Lohr. "DNA sequence-dependent variation in nucleosome structure, stability, and dynamics detected by a FRET-based analysisThis paper is one of a selection of papers published in this Special Issue, entitled 29th Annual International Asilomar Chromatin and Chromosomes Conference, and has undergone the Journal’s usual peer review process." Biochemistry and Cell Biology 87, no. 1 (February 2009): 323–35. http://dx.doi.org/10.1139/o08-126.

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Förster resonance energy transfer (FRET) techniques provide powerful and sensitive methods for the study of conformational features in biomolecules. Here, we review FRET-based studies of nucleosomes, focusing particularly on our work comparing the widely used nucleosome standard, 5S rDNA, and 2 promoter-derived regulatory element-containing nucleosomes, mouse mammary tumor virus (MMTV)-B and GAL10. Using several FRET approaches, we detected significant DNA sequence-dependent structure, stability, and dynamics differences among the three. In particular, 5S nucleosomes and 5S H2A/H2B-depleted nucleosomal particles have enhanced stability and diminished DNA dynamics, compared with MMTV-B and GAL10 nucleosomes and particles. H2A/H2B-depleted nucleosomes are of interest because they are produced by the activities of many transcription-associated complexes. Significant location-dependent (intranucleosomal) stability and dynamics variations were also observed. These also vary among nucleosome types. Nucleosomes restrict regulatory factor access to DNA, thereby impeding genetic processes. Eukaryotic cells possess mechanisms to alter nucleosome structure, to generate DNA access, but alterations often must be targeted to specific nucleosomes on critical regulatory DNA elements. By endowing specific nucleosomes with intrinsically higher DNA accessibility and (or) enhanced facility for conformational transitions, DNA sequence-dependent nucleosome dynamics and stability variations have the potential to facilitate nucleosome recognition and, thus, aid in the crucial targeting process. This and other nucleosome structure and function conclusions from FRET analyses are discussed.
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Szerlong, Heather J., and Jeffrey C. Hansen. "Nucleosome distribution and linker DNA: connecting nuclear function to dynamic chromatin structureThis paper is one of a selection of papers published in a Special Issue entitled 31st Annual International Asilomar Chromatin and Chromosomes Conference, and has undergone the Journal’s usual peer review process." Biochemistry and Cell Biology 89, no. 1 (February 2011): 24–34. http://dx.doi.org/10.1139/o10-139.

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Genetic information in eukaryotes is managed by strategic hierarchical organization of chromatin structure. Primary chromatin structure describes an unfolded nucleosomal array, often referred to as “beads on a string”. Chromatin is compacted by the nonlinear rearrangement of nucleosomes to form stable secondary chromatin structures. Chromatin conformational transitions between primary and secondary structures are mediated by both nucleosome-stacking interactions and the intervening linker DNA. Chromatin model system studies find that the topography of secondary structures is sensitive to the spacing of nucleosomes within an array. Understanding the relationship between nucleosome spacing and higher order chromatin structure will likely yield important insights into the dynamic nature of secondary chromatin structure as it occurs in vivo. Genome-wide nucleosome mapping studies find the distance between nucleosomes varies, and regions of uniformly spaced nucleosomes are often interrupted by regions of nonuniform spacing. This type of organization is found at a subset of actively transcribed genes in which a nucleosome-depleted region near the transcription start site is directly adjacent to uniformly spaced nucleosomes in the coding region. Here, we evaluate secondary chromatin structure and discuss the structural and functional implications of variable nucleosome distributions in different organisms and at gene regulatory junctions.
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Clapier, Cedric R., Gernot Längst, Davide F. V. Corona, Peter B. Becker, and Karl P. Nightingale. "Critical Role for the Histone H4 N Terminus in Nucleosome Remodeling by ISWI." Molecular and Cellular Biology 21, no. 3 (February 1, 2001): 875–83. http://dx.doi.org/10.1128/mcb.21.3.875-883.2001.

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ABSTRACT The ATPase ISWI can be considered the catalytic core of several multiprotein nucleosome remodeling machines. Alone or in the context of nucleosome remodeling factor, the chromatin accessibility complex (CHRAC), or ACF, ISWI catalyzes a number of ATP-dependent transitions of chromatin structure that are currently best explained by its ability to induce nucleosome sliding. In addition, ISWI can function as a nucleosome spacing factor during chromatin assembly, where it will trigger the ordering of newly assembled nucleosomes into regular arrays. Both nucleosome remodeling and nucleosome spacing reactions are mechanistically unexplained. As a step toward defining the interaction of ISWI with its substrate during nucleosome remodeling and chromatin assembly we generated a set of nucleosomes lacking individual histone N termini from recombinant histones. We found the conserved N termini (the N-terminal tails) of histone H4 essential to stimulate ISWI ATPase activity, in contrast to other histone tails. Remarkably, the H4 N terminus, but none of the other tails, was critical for CHRAC-induced nucleosome sliding and for the generation of regularity in nucleosomal arrays by ISWI. Direct nucleosome binding studies did not reflect a dependence on the H4 tail for ISWI-nucleosome interactions. We conclude that the H4 tail is critically required for nucleosome remodeling and spacing at a step subsequent to interaction with the substrate.
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Knezetic, J. A., G. A. Jacob, and D. S. Luse. "Assembly of RNA polymerase II preinitiation complexes before assembly of nucleosomes allows efficient initiation of transcription on nucleosomal templates." Molecular and Cellular Biology 8, no. 8 (August 1988): 3114–21. http://dx.doi.org/10.1128/mcb.8.8.3114-3121.1988.

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We have previously shown that assembly of nucleosomes on the DNA template blocks transcription initiation by RNA polymerase II in vitro. In the studies reported here, we demonstrate that assembly of a complete RNA polymerase II preinitiation complex before nucleosome assembly results in nucleosomal templates which support initiation in vitro as efficiently as naked DNA. Control experiments prove that our observations are not the result of slow displacement of nucleosomes by the transcription machinery during chromatin assembly, nor are they an artifact of inefficient nucleosome deposition on templates already bearing an RNA polymerase. Thus, the RNA polymerase II preinitiation complex appears to be resistant to disruption by subsequent nucleosome assembly.
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Anderson, J. D., and J. Widom. "Poly(dA-dT) Promoter Elements Increase the Equilibrium Accessibility of Nucleosomal DNA Target Sites." Molecular and Cellular Biology 21, no. 11 (June 1, 2001): 3830–39. http://dx.doi.org/10.1128/mcb.21.11.3830-3839.2001.

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ABSTRACT Polypurine tracts are important elements of eukaryotic promoters. They are believed to somehow destabilize chromatin, but the mechanism of their action is not known. We show that incorporating an A16 element at an end of the nucleosomal DNA and further inward destabilizes histone-DNA interactions by 0.1 ± 0.03 and 0.35 ± 0.04 kcal mol−1, respectively, and is accompanied by 1.5- ± 0.1-fold and 1.7- ± 0.1-fold increases in position-averaged equilibrium accessibility of nucleosomal DNA target sites. These effects are comparable in magnitude to effects of A16 elements that correlate with transcription in vivo, suggesting that our system may capture most of their physiological role. These results point to two distinct but interrelated models for the mechanism of action of polypurine tract promoter elements in vivo. Given a nucleosome positioned over a promoter region, the presence of a polypurine tract in that nucleosome's DNA decreases the stability of the DNA wrapping, increasing the equilibrium accessibility of other DNA target sites buried inside that nucleosome. Alternatively (if nucleosomes are freely mobile), the presence of a polypurine tract provides a free energy bias for the nucleosome to move to alternative locations, thereby changing the equilibrium accessibilities of other nearby DNA target sites.
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Gangaraju, Vamsi K., and Blaine Bartholomew. "Dependency of ISW1a Chromatin Remodeling on Extranucleosomal DNA." Molecular and Cellular Biology 27, no. 8 (February 5, 2007): 3217–25. http://dx.doi.org/10.1128/mcb.01731-06.

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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.
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Dissertations / Theses on the topic "Nucleosome in the cell"

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Deniz, Ozgen. "Nucleosome Positioning in Budding Yeast = Posicionamiento de nucleosomas en Saccharomyces cerevisiae." Doctoral thesis, Universitat de Barcelona, 2014. http://hdl.handle.net/10803/145763.

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The nucleosome is the fundamental structural unit of DNA compaction in eukaryotic cells and is formed by the wrapping of 147 bp double stranded DNA around a histone octamer. Nucleosome organization plays a major role in controlling DNA accessibility to regulatory proteins, hence affecting cellular processes such as transcription, DNA replication and repair. Our study focuses on genome-wide nucleosome positioning in S. cerevisiae to explore nucleosome determinants and plasticity throughout the cell cycle and their interplay with gene expression based on cell mRNA abundance. We pursued the contribution of DNA physical properties on nucleosome organization around key regulatory regions such as TSSs and TTSs by analyzing genome-wide MNase-digestion profile of genomic DNA. We also implemented a systematic approach to standardize MNase-Seq experiments by minimizing the noise generated by extrinsic factors to enable an accurate analysis of the underlying principles of nucleosome positioning and dynamics. Moreover, we carried out a large-scale study of nucleosome plasticity throughout the cell cycle and its interplay with transcription based on a comparative analysis among nucleosome maps, gene expression data and MNase sensitivity assays. We then focused on nucleosome organization around DNA replication origins and its possible effect on origin activation. Finally, we sought to characterize centromeric nucleosome composition and its oscillation along cell cycle. During the course of these studies, we found that key regulatory regions such as 5’ and 3’ nucleosome free regions (NFRs) contain unusual physical properties that are intrinsic to genomic DNA. We further demonstrated that DNA physical properties and transcription factors act synergistically to define NFRs, especially in genes with an open promoter structure. Once NFR is defined, the nucleosome positioning around TSSs can be predicted by a simple statistical model, supporting the energy barrier model for nucleosome positioning determination. However, we also observed that nucleosomes are quite dynamic at distal 5’ NFRs and do have distinct regulatory mechanisms. Our comparative analysis of nucleosome organization along cell cycle revealed that chromatin exhibits a distinct configuration due to DNA replication-dependent organization at S phase, showing higher sensitivity to MNase and displaying fuzzier nucleosomes along the genome. Moreover, we observed different features at M phase, where chromatin compaction is the highest and displays a slightly different pattern than in G1 and G2 phases. Interestingly, these changes in chromatin organization are sudden and acute and only affect some regions of the genome, whereas the majority of genes present conserved nucleosome patterns along cell cycle. Our individual gene analysis disclosed that the largest changes take place in cell cycle-dependent genes, indicating the interplay between chromatin and transcription. Moreover, a distinct nucleosome organization at high and low transcription rates further supports this relationship. The detailed analysis around replication origins shows that they display slightly wider NFRs at G1 phase due to pre-Replication complex binding. Once the replication origins are active, nucleosomes partially occupy NFRs up to a certain extent due to constitutive binding of ORC. Moreover, we provided further evidence that early firing origins tend to have more ordered nucleosome organization than late firing origins. Finally we illustrated that centromeric nucleosomes display a perfect positioning, confirming their strong centromeric sequence-dependent recruitment to DNA. The characterization of histone composition under physiological cell conditions suggested that the octameric nucleosome assembly model is favored in centromeres. Yet, our analysis along cell cycle showed centromeric nucleosome dynamics, proposing that its composition might oscillate along cell cycle. Taken together, our accurate study provides a dynamic picture of nucleosome positioning and its determinants; new insights into cell cycle-dependent chromatin organization on key regulatory regions and its interplay with gene expression; and adds a new dimension to the characterization of centromeric nucleosomes.
Nuestro estudio se centra en el posicionamiento de nucleosomas a nivel genómico en levadura, con tal de explorar los factores determinantes de nucleosomas y su plasticidad a lo largo del ciclo celular, así como su relación con la expresión génica basándonos en la cantidad de mARN celular. Encontramos que las regiones libres de nucleosomas (NFRs en inglés) en 5’ y 3’ contienen propiedades físicas inusuales, las cuales son intrínsecas del ADN genómico. Además, demostramos que estas propiedades físicas actúan sinérgicamente con factores de transcripción para definir las NFRs. Una vez la NFR está definida, el posicionamiento de nucleosomas en torno al inicio de transcripción (TSS en inglés) puede predecirse con modelos estadísticos simples. No obstante, también observamos que los nucleosomas son bastante dinámicos en las regiones distales a 5’NFRs y poseen distintos mecanismos reguladores. Nuestro análisis comparativo acerca de la organización de los nucleosomas reveló que la cromatina de hecho exhibe una configuración distinta debido al reordenamiento dependiente de la replicación en fase S, mostrando una mayor sensibilidad de corte por el enzima MNase y un mayor número de nucleosomas deslocalizados a lo largo del genoma. Adicionalmente, observamos características particulares en fase M, donde la cromatina sufre un mayor grado de compactación. Notablemente, estos cambios en la organización de la cromatina son repentinos y agudos y sólo afectan a algunas regiones del genoma, mientras que la mayoría de genes presentan una conservación del patrón de nucleosomas a lo largo del ciclo celular. El análisis detallado en torno a los orígenes de replicación muestra una NFR más ancha en fase G1, debido a la unión del complejo pre-replicatorio. Una vez se activa el origen, los nucleosomas sólo ocupan parcialmente la NFR, debido a la unión constitutiva del complejo de origen de replicación (ORC en inglés). También proporcionamos evidencias de que los orígenes tempranos tienden a tener una organización nucleosomal más ordenada que los tardíos. Finalmente, ilustramos que los nucleosomas centroméricos poseen un posicionamiento idóneo y asimismo, un ensamblaje distinto. Sin embargo, nuestro análisis también mostró la dinámica de los nucleosomas centroméricos a lo largo del ciclo celular, indicando que de hecho su composición puede oscilar a lo largo del ciclo celular. En conjunto, nuestro detallado estudio proporciona una imagen dinámica del posicionamiento de nucleosomas y sus factores determinantes; nuevos indicios respecto a la organización de la cromatina en regiones reguladoras clave en base al ciclo celular y su conexión con la expresión génica; y finalmente, añade una nueva dimensión a la caracterización de los nucleosomas centroméricos.
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Wight, Andrew. "Adaptive NK Cell Memory and Nucleosome Interference: Two Tales of the Ly49 Receptor Family." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/37059.

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Ly49 receptors are the canonical natural killer cell class-I major histocompatibility complex receptors expressed in mice. They have a well-defined role in natural killer cell self/non-self discrimination and in the developmental licensing of functional natural killer cells. In this thesis, I report two novel aspects of Ly49 receptor biology. First, I show that their expression may be regulated by specific nucleosome occupancy on AML-1 binding sites within the distal Ly49 promoter. This finding sheds light on a potential regulatory pathway that has thus far been unexplored in studies of the Ly49 receptor family, and highlights the Ly49 family as an ideal model system in which to study the impact of nucleosome occupancy in general. Second, I show that Ly49 receptors have a central and indispensable role in the emerging phenomenon known as adaptive natural killer cell memory. Natural killer cells have recently been observed displaying adaptive, long-lived, antigen specific memory responses comparable to T cell memory responses, but no explanatory mechanism has been discovered to describe how adaptive memory is possible in these ‘innate’ immune cells. Using Ly49-deficient mice, I show that the inhibitory, self-specific Ly49 receptors Ly49C and Ly49I are required for adaptive memory responses to chemical haptens or protein antigens. Moreover, I show that Ly49C/I binding capabilities are required during all stages of the memory response, as is antigen presentation in the context of class I major histocompatibility complex, again analogous to T cell memory responses. I present initial findings implicating these Ly49 receptors as key components of the antigen recognition process itself, and propose a mechanism based in evolutionarily ancient immunology to explain how this specificity could arise. Finally, I demonstrate that Ly49-dependent natural killer cell memory is capable of mediating powerful anti-cancer vaccination effects using an aggressive model of melanoma. Together, these findings in Ly49 family expression regulation and its functional role in adaptive NK cell responses open several new avenues of study in Ly49 receptor biology and natural killer cell immunology.
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Koorsen, Gerrit. "The association of the secondary DNA-binding site of linker histone H5 in a nucleosome." Master's thesis, University of Cape Town, 2001. http://hdl.handle.net/11427/4282.

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Bibliography: leaves 153-170.
In order to understand the role of linker histones in the formation of the 30-run chromatin fibre as well as their role in transcriptional repression, it is essential to know their location on the nucleosome. In this study, we have modelled the location of the globular domain of chicken linker histone HS (GHS) on the nuc1eosome. The primary DNA binding site of GH5 was modelled by homology to the co-crystal structure of the E. coli CAP-DNA complex.
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FENG, YIHONG. "Controllable cell delivery and chromatin structure observation using DNA nanotechnology." Kyoto University, 2020. http://hdl.handle.net/2433/258987.

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Cook, April D. "Characterization of nucleosome occupancy in mammalian cells." Thesis, Harvard University, 2014. http://nrs.harvard.edu/urn-3:HUL.InstRepos:13070019.

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Chromatin is a complex of genomic DNA, RNA, and associated proteins. Many of the processes that occur on chromatin regulate the accessibility of the genetic material of a cell. The nucleosome is the basic subunit of chromatin, composed of a histone octamer wrapped with approximately 150bp of DNA. Alterations to chromatin structure, including to nucleosomes and their location, underlie global transcriptional diversity. A striking example of this is the so-called "open" chromatin state in pluripotent cells, characterized by loosely bound chromatin proteins and rapid nucleosome turnover, that allows transcriptional flexibility for subsequent differentiation. In contrast, differentiated cells contain compacted chromatin that can selectively block access to DNA and subsequent transcription. Thus, characterizing the physical state of chromatin is important to understanding its regulatory state. Digestion of chromatin with micrococcal nuclease (MNase) and subsequent sequencing of the protected DNA fragments produces a map of nucleosome occupancy. Traditional MNase mapping experiments capture a snapshot of nucleosome occupancy, providing information about nucleosomes that are accessible at the level of digestion used. We analyzed regions of difference in nucleosome occupancy between embryonic stem cells (ESCs), induced pluripotent stem cells (iPSCs) and differentiated cell types using traditional MNase-seq and found that differences in pluripotent and differentiated cells are punctate and correlate with regulatory regions important for pluripotency and development. Further, our analysis shows ESCs and iPSCs to be vastly more similar to each other in their chromatin structure than to the differentiated cells. We then developed a new way of collecting and analyzing MNase-seq data that allows us to determine both nucleosome occupancy as well as the accessibility of DNA to regulatory factors. Our methodology discerns distinct physical states of chromatin and provides novel insights into the accessibility of regulatory regions. Additionally, we present a quantitative metric useful for characterizing local and global regions of the genome that should be useful in future cell type comparisons.
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Pohl, Andy 1979. "Nucleosome dynamics and analysis in breast cancer cells." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/328416.

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Genome-wide analysis of the nucleosome positioning and histone H1 isoform content of the T47D breast cancer cell line has found a number of observations, namely that with a gentle digestion of microccocal nuclease (MNase), a nucleosome is visible just upstream of the transcription start site, in the region known as the “nucleosome-free region” (NFR). H1 isoforms bind to chromatin mainly in a redundant manner, but H1.2 and H1.3 show some specificity while H1.5 increases its binding dramatically after a progesterone stimulus. In the course of these studies, a general-purpose software package was developed for the manipulation and analysis of bigWig files, a data format for storing continuous signal data assigned to genome coordinates
En el meu estudi genòmic sobre el posicionament de nucleosomes i sobre elcontingut de les isoformes de la histona H1 en cèl•lules de càncer de mama T47D he dut a terme una sèrie d'observacions. Específicament he trobat que amb una digestió suau amb nucleasa micrococcal, es pot identificar un nucleosoma just abans del lloc d'inici de transcripció, en la regió coneguda com a "regió lliure de nucleosomes". També he vist que les diferents isoformes somàtiques de la histona H1 (H1.0-H1.5, H1x) s'uneixen a la cromatina de manera redundant, però que la H1.2 i la H1.3 presenten certa especificitat, mentre que la H1.5 mostra un augment de la unió generalitzat després d'estimular les cèl•lules amb progesterona. En el decurs de la meva recerca, he desenvolupat un programari general per la manipulació i l'anàlisi d'arxius amb format bigWig, un format per a l'emmagetzematge de dades de senyals continus al llarg de les coordenades del genoma.
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Gatta, R. "Chromatin configuration of CCAAT-containing cell cycle promoters." Doctoral thesis, Università degli Studi di Milano, 2009. http://hdl.handle.net/2434/158416.

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The CCAAT box is a frequent promoter element bound by NF-Y, a trimer with H2A-H2B-like subunits. We developed a MNase I-based ChIP protocol on homogeneous cell populations to study cell-cycle promoters at the single nucleosome level. We analyzed histone acetylations and methylations and the association of enzymatic activities. This thesis presents different novel findings. The first finding was that H3-H4 take part of core promoters under active conditions, with the expected cohort of “positive” modifications, while H2A-H2B are removed and substituted by NF-Y. Through the use of a dominant negative mutant we show also that NF-Y is important for H3K36me3 deposition and for Pol II elongation. The second finding was that H3K4 methylations are highly dynamic and H3K4me1 is a crucial positive mark. Both functional and pharmacological inactivation led to state that KDM1 plays a positive role in transcription of G2/M genes. It requires CoREST, which is recruited on active promoters through direct interactions with NF-Y. Therefore, these preliminary data are the first in vivo indication of a crucial interplay between core histones and “deviant” histone-fold such as NF-Y, leading to fine tuning of histone methylations. The third finding was that NF-Y is not involved in histone acetyl-marks deposition as well as in histone methyl-marks: in fact, histone acetylation status of active cell cycle genes was only slightly perturbed after NF-Y removal. Moreover, this work proposed a special histone acetylation pattern typical of cell cycle gene cluster, characterized by H2BK120ac and H3K9,18,36ac deposited on H3 in repressive conditions. And finally, by in vivo analysis we showed GCN5 and PCAF involvement in the acetyl-marks deposition, and the probable NF-Y dependent recruitment of multisubunit complexes responsible of the chromatin remodelling, like STAGA and ATAC.
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Garza, Manero Sylvia Patricia. "The role of high mobility group of nucleosome binding proteins in stem cell biology and differentiation." Thesis, University of Glasgow, 2019. http://theses.gla.ac.uk/41111/.

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The high mobility group of nucleosome binding proteins (HMGNs) are chromatin architectural proteins that bind specifically to nucleosomes and influence chromatin structure and DNA-dependent functions. However, the mechanisms underlying these events remain largely unknown. HMGN1 and HMGN2 are highly expressed by embryonic stem cells and are downregulated as differentiation proceeds. Nevertheless, embryonic and adult neural stem cells retain elevated levels of these proteins. Chromatin plasticity is essential for the pluri- and multipotency of stem cells and it is achieved by maintaining an open and dynamic chromatin conformation. Conversely, developmental potential seems to be restricted by chromatin condensation. The present work shows that loss of HMGN1 or HMGN2 in pluripotent embryonal carcinoma cells leads to increased spontaneous neuronal differentiation, which is accompanied by a reduction in pluripotency markers and higher gene expression of lineage-specific transcription factors. Inhibition of signalling pathways relevant for neurogenesis does not re-establish the phenotype observed in Hmgn2-knockout cells. Withdrawal of the factors sustaining pluripotency in embryonal carcinoma cells results in higher induction of pro-neural factors in cells lacking HMGN1 or HMGN2. Neural stem cells derived from Hmgn-knockout cells also display higher gene expression of pro-neural transcription factors and increased spontaneous neuronal differentiation. Loss of HMGN2 disrupts the active histone modification landscape, and therefore affects the chromatin structure at local and global levels. The proposition is that the local changes directly influence the transcription rates of pluripotency and lineage-specific transcription factors, while the global changes may restrict chromatin plasticity. The present data support a hypothesis whereby HMGNs contribute to the chromatin plasticity of stem cells by promoting an active histone modification landscape and open chromatin conformation, which are essential for preserving the self-renewal and developmental potential of stem cells.
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Pünzeler, Sebastian [Verfasser], and Sandra [Akademischer Betreuer] Hake. "PWWP2A : a novel H2A.Z nucleosome interactor involved in cell cycle regulation / Sebastian Pünzeler. Betreuer: Sandra Hake." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2015. http://d-nb.info/1111505349/34.

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Unhavaithaya, Yingdee. "Conserved Nucleosome Remodeling/Histone Deacetylase Complex and Germ/Soma Distinction in C. elegans: A Dissertation." eScholarship@UMMS, 2003. https://escholarship.umassmed.edu/gsbs_diss/239.

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A rapid cascade of regulatory events defines the differentiated fates of embryonic cells, however, once established, these differentiated fates and the underlying transcriptional programs can be remarkably stable. Here, we describe two proteins, MEP-1, a novel protein, and LET-418/Mi-2, both of which are required for the maintenance of somatic differentiation in C. elegans. MEP-1 was identified as an interactor of PIE-1, a germ-specific protein required for germ cell specification, while LET-418 is a protein homologous to Mi-2, a core component of the nuc1eosome remodeling/histone deacetylase (NuRD) complex. In animals lacking MEP-1 and LET-418, germline-specific genes become derepressed in somatic cells, and Polycomb group (PcG) and SET domain-related proteins promote this ectopic expression. We demonstrate that PIE-1 forms a complex with MEP-1, LET-418, and HDA-1. Furthermore, we show that the overexpression of PIE-1 can mimic the mep-1/let-418 phenotype, and that PIE-1 can inhibit the Histone deacetylase activity of the HDA-1 complex in COS cells. Our findings support a model in which PIE-1 transiently inhibits MEP-1 and associated factors to maintain the pluripotency of germ cells, while at later times MEP-1 and LET-418 remodel chromatin to establish new stage- or cell-type-specific differentiation potential.
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Books on the topic "Nucleosome in the cell"

1

Kornberg, Roger D. The nucleosome. Preston: Lancashire Polytechnic.Library and Learning Resources Service, 1988.

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McQuibban, Angus. Yeast nucleosome and chromatin assembly. Ottawa: National Library of Canada, 1995.

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van, Driel Roeland, and Otte Arie P, eds. Nuclear organization, chromatin structure, and gene expression. Oxford: Oxford University Press, 1997.

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Zabal, Monique M. Preparation of nucleosome core particles for electron microscopy. Ottawa: National Library of Canada, 1990.

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Stone, Graham Robert. Studies of the nucleosome core particle structure in Physarum polycephalum. Portsmouth: Portsmouth Polytechnic, Dept. of Biological Sciences, 1985.

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Baudino, Troy A., ed. Cell-Cell Interactions. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-604-7.

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Baluska, Frantisek, Dieter Volkmann, and Peter W. Barlow. Cell-Cell Channels. New York, NY: Springer New York, 2006. http://dx.doi.org/10.1007/978-0-387-46957-7.

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J, Nelson W., and Fuchs Elaine, eds. Cell-cell junctions. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2010.

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J, Nelson W., and Fuchs Elaine, eds. Cell-cell junctions. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2010.

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Turksen, Kursad, ed. Stem Cell Renewal and Cell-Cell Communication. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1570-6.

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Book chapters on the topic "Nucleosome in the cell"

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Längst, Gernot, Vladimir B. Teif, and Karsten Rippe. "Chromatin Remodeling and Nucleosome Positioning." In Genome Organization and Function in the Cell Nucleus, 111–38. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527639991.ch5.

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Rippe, Karsten. "The Folding of the Nucleosome Chain." In Genome Organization and Function in the Cell Nucleus, 139–67. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527639991.ch6.

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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro, and Anton Wutz. "Chromatin Dynamics." In Introduction to Epigenetics, 29–47. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_2.

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AbstractThe nucleus of a eukaryotic cell is a very busy place. Not only during replication of the DNA, but at any time in the cell cycle specific enzymes need access to genetic information to process reactions such as transcription and DNA repair. Yet, the nucleosomal structure of chromatin is primarily inhibitory to these processes and needs to be resolved in a highly orchestrated manner to allow developmental, organismal, and cell type-specific nuclear activities. This chapter explains how nucleosomes organize and structure the genome by interacting with specific DNA sequences. Variants of canonical histones can change the stability of the nucleosomal structure and also provide additional epigenetic layers of information. Chromatin remodeling complexes work locally to alter the regular beads-on-a-string organization and provide access to transcription and other DNA processing factors. Conversely, factors like histone chaperones and highly precise templating and copying mechanisms are required for the reassembly of nucleosomes and reestablishment of the epigenetic landscape after passage of activities processing DNA sequence information. A very intricate molecular machinery ensures a highly dynamic yet heritable chromatin template.
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Aarbakke, Jarle, Per S. Prytz, Peter K. Chiang, and Atle Bessesen. "Differentiation of Human Leukemia Cells by Nucleoside Analogues." In Tumor Cell Differentiation, 241–49. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4594-0_17.

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Smerdon, Michael J. "DNA Excision Repair at the Nucleosome Level of Chromatin." In DNA Repair Mechanisms and Their Biological Implications in Mammalian Cells, 271–94. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-1327-4_26.

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Gandhi, Varsha, and Pier Luigi Zinzani. "Nucleoside Analogs in the Therapy of T-Cell Malignancies." In T-Cell Lymphomas, 263–78. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-170-7_15.

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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro, and Anton Wutz. "Cellular Memory." In Introduction to Epigenetics, 49–66. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_3.

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AbstractThe identity of cells in an organism is largely defined by their specific transcriptional profile. During cell division, these profiles need to be faithfully inherited to the daughter cells to ensure the maintenance of cell structure and function in a cell lineage. Here, you will learn how two groups of chromatin regulators, the Polycomb group (PcG) and the Trithorax group (TrxG), act in an antagonistic manner to maintain differential gene expression states. Members of the PcG cooperate in large multiprotein complexes to modify histones with repressive marks, resulting in condensed chromatin domains. Conversely, the TrxG proteins counteract the repressed domains by opening nucleosomal structures and establishing activating histone modifications. PcG and TrxG proteins are evolutionary highly conserved and control diverse processes, such as the identity of stem cells in mammalian development to the process of vernalization in plants.
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Jarvis, Simon M. "Chemical and Molecular Probes of Nucleoside Transport Mechanisms in Mammalian Tissues." In Cell Membrane Transport, 399–421. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-9601-8_20.

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Saven, Alan, and Lawrence D. Piro. "Treatment of Hairy Cell Leukemia with Nucleoside Analogs." In Nucleoside Analogs in Cancer Therapy, 227–46. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003067634-9.

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Schächner, Christopher, Philipp E. Merkl, Michael Pilsl, Katrin Schwank, Kristin Hergert, Sebastian Kruse, Philipp Milkereit, Herbert Tschochner, and Joachim Griesenbeck. "Establishment and Maintenance of Open Ribosomal RNA Gene Chromatin States in Eukaryotes." In Ribosome Biogenesis, 25–38. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2501-9_2.

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AbstractIn growing eukaryotic cells, nuclear ribosomal (r)RNA synthesis by RNA polymerase (RNAP) I accounts for the vast majority of cellular transcription. This high output is achieved by the presence of multiple copies of rRNA genes in eukaryotic genomes transcribed at a high rate. In contrast to most of the other transcribed genomic loci, actively transcribed rRNA genes are largely devoid of nucleosomes adapting a characteristic “open” chromatin state, whereas a significant fraction of rRNA genes resides in a transcriptionally inactive nucleosomal “closed” chromatin state. Here, we review our current knowledge about the nature of open rRNA gene chromatin and discuss how this state may be established.
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Conference papers on the topic "Nucleosome in the cell"

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Li, Zhaoyu. "Abstract A34: Nucleosome dynamics of cell differentiation." In Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-a34.

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Takami, Tomohide, Jun-ichi Uewaki, Hiroshi Ochiai, Masato Koyama, Yoshihide Ogawa, Mikako Saito, Hideaki Matsuoka, and Shin-ichi Tate. "Live Dynamics on Femtoinjection of GFP-Tagged Nucleosome Chaperones into HeLa Cell." In JSAP-OSA Joint Symposia. Washington, D.C.: OSA, 2014. http://dx.doi.org/10.1364/jsap.2014.18p_c4_12.

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Krause, Hans, Odiljon Ikromov, Eymad All Kamal, Kurt Miller, Martin Schostak, and Burkhard Jandrig. "Abstract 2170: The SWI/SNF nucleosome-remodeling gene PBRM1 - Another tumor suppressor gene in renal cell carcinomas." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2170.

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Doebley, Anna-Lisa, Hanna Liao, Caroline Kikawa, Eden Cruikshank, Minjeong Ko, Anna Hoge, Joseph Hiatt, et al. "Abstract LB022: Griffin: A method for nucleosome profiling and breast cancer subtype prediction from ultra-low pass whole genome sequencing of cell-free DNA." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-lb022.

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Markus, Havell, Jun Zhao, Tania Contente-Cuomo, Elizabeth Raupach, Ahuva Odenheimer-Bergman, Sydney Connor, Bradon McDonald, et al. "Abstract PR14: Sub-nucleosomal fragmentation in urine cell-free DNA." In Abstracts: AACR Special Conference on Advances in Liquid Biopsies; January 13-16, 2020; Miami, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.liqbiop20-pr14.

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Karande, S., A. Urazova, J. Balbach, G. Szabó, and A. Simm. "New Identified Posttranslational Modified (Glycated) Lysines and Arginines in Histones in Aging Human Heart/Endothelial Cells: Impact on Histone Octamer and Nucleosome Stability." In 52nd Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2023. http://dx.doi.org/10.1055/s-0043-1761691.

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Cerdà Moncadas, Maria, Núria Toledo Pons, Monica De la Peña Bravo, Josep Miquel Bauçà Rosselló, Laura Fueyo Ramírez, Dani Morell García, Javier Pierola Lopetegui, Maria Paloma Gimenez Carrero, and Antonia Barceló Bennasar. "Cell-free DNA and nucleosomes are increased in sera of patients with Obstructive Sleep Apnoea." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa1757.

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Liu, Xiaojun, Billie Nowak, Yingjun Jiang, Walter Hittelman, and William Plunkett. "Abstract 3418: Mechanism of cell death induced by the DNA strand-breaking nucleoside analogue CNDAC." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3418.

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Oubounyt, Mhaned, Zakaria Louadi, and Kil To Chong. "Prediction of Nucleosome Forming and Nucleosome Inhibiting DNA Sequences Using Convolutional Neural Networks." In 2019 International Conference on Wireless Technologies, Embedded and Intelligent Systems (WITS). IEEE, 2019. http://dx.doi.org/10.1109/wits.2019.8723783.

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Borisov, Valery Alexandrovich, Boris Ivanovich Sanin, Svetlana Evgenievna Samsonova, Nikolaevna Harutyunyan Elena, and Borisovna Golubeva Dina. "THE EXPERIENCE OF DOMESTIC ANTIVIRAL AGENTS, AND SOME OF OWN APPROACHES IN THE TREATMENT OF CHRONIC HEPATITIS C IN ADULTS." In Themed collection of papers from Foreign intemational scientific conference «Joint innovation - joint development». Medical sciences . Part 2. Ьу НNRI «National development» in cooperation with PS of UA. June 2023. Crossref, 2023. http://dx.doi.org/10.37539/230629.2023.19.61.022.

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In the management of 148 adult patients with chronic hepatitis C (CHC) of both sexes without special selection (taken into account only absolute contraindications to its performance) there were used domestic basic antiviral drugs - BAD| (short-living interferons (IFN) α, interferon inducers and nucleoside analogues) in parallel with additional antiviral drugs (drug glycyrrhizinic acid or amantadine) and maintenance therapy (stimulators of T-cell immunity and means of correction of side effects). Treatment was carried out in the framework of the developed complex of principles and approaches including in part, the formation of the starting average weekly dose of interferon IFN with accounting of the character of interferon status of the patient, a gradual increase in the average weekly dose of interferon IFN during the course of therapy, the delayed use of nucleoside analogs and others. As a result, against the background of a significant reduction in financial expenses and the aggressiveness of treatment the stable positive therapeutic outcome in the general population of patients occurred in 92.6%, with 87.2% in patients with genotype (G) 1.
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Reports on the topic "Nucleosome in the cell"

1

Zlatanova, Jordanka. BRCA 1-Mediated Histone Monoubiquitylation: Effect on Nucleosome Dynamics. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada482568.

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Howell, Steven C. Dynamic Conformations of Nucleosome Arrays in Solution from Small-Angle X-ray Scattering. Office of Scientific and Technical Information (OSTI), January 2016. http://dx.doi.org/10.2172/1338475.

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Byers, Stephen W. Cell-Cell Adhesion and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2000. http://dx.doi.org/10.21236/ada395237.

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Byers, Stephen W. Cell-Cell Adhesion and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 1999. http://dx.doi.org/10.21236/ada371168.

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Byers, Stephen W. Cell-Cell Adhesion and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 1998. http://dx.doi.org/10.21236/ada345188.

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Williams, Thomas. Cell Biology Boardgame: Cell Survival: Transport. University of Dundee, March 2023. http://dx.doi.org/10.20933/100001281.

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Get your mRNAs from one side of the cell to the other so they can be turned into protein. Fastest wins! This game takes a fun approach to detail findings from real life research. Great for 2-5 people age 3+, lasts around 15 mins per game.
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Baker, Nicholas E. Cell Proliferation, Cell Death, and Size Regulation. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/adb248354.

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Williams, Thomas. Cell Biology Board Game: Cell Survival Drive. University of Dundee, 2023. http://dx.doi.org/10.20933/100001276.

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When dangers strike a cell, they are detected by sensors. Sensors tell messengers about the danger. Messengers tell the organiser. The organiser plans the cell defence, using responders and recyclers. Researchers in the MRC-PPU are figuring out how these different parts interact with each other.
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Williams, Thomas. Cell Biology Board Game: Cell Survival (Home Version). University of Dundee, 2022. http://dx.doi.org/10.20933/100001271.

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Williams, Thomas. Cell Biology Board Game: Cell Survival (School Version). University of Dundee, 2022. http://dx.doi.org/10.20933/100001270.

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Cells are the smallest units of life. The environment around cells is always changing. Cells need to adapt to survive. This curriculum linked game and lesson plan introduces the world of cells to pupils 8-13. But can they keep their cells alive? This is a guide to how the cell survival resources can be used in a lesson and can be adapted as the teacher sees fit to do so. This lesson is aimed at 8-13 year olds, and fits into an hour long session. The Cell Survival Game has been adapted for both home use and for use in the classroom, and is accompanied by a series of videos. Learning Outcomes – Cells are the smallest unit of life – There are many different types of cells, and some examples of cell types – Cells experience many dangers, and some examples of dangers – How cells notice and defend themselves against dangers Links to the Curriculum – Health and Wellbeing: I am developing my understanding of the human body – Languages: I can find specific information in a straight forward text (book and instructions) to learn new things, I discover new words and phrases (relating to cells) – Mathematics: I am developing a sense of size and amount (by using the dice), I am exploring number processes (addition and subtraction) and understand they represent quantities (steps to finish line), I am learning about measurements (cell sizes) and am exploring patterns (of cell defences against dangers) – Science: I am learning about biodiversity (different types of microbes), body systems, cells and how they work. – Technology: I am learning about new technologies (used to understand how cells work).
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