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Journal articles on the topic 'Chromatin'

Author: Grafiati

Published: 4 June 2021

Last updated: 27 July 2024

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1

Mishra, Prashant K., Sultan Ciftci-Yilmaz, David Reynolds, Wei-Chun Au, Lars Boeckmann, Lauren E. Dittman, Ziad Jowhar, et al. "Polo kinase Cdc5 associates with centromeres to facilitate the removal of centromeric cohesin during mitosis." Molecular Biology of the Cell 27, no. 14 (July 15, 2016): 2286–300. http://dx.doi.org/10.1091/mbc.e16-01-0004.

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Sister chromatid cohesion is essential for tension-sensing mechanisms that monitor bipolar attachment of replicated chromatids in metaphase. Cohesion is mediated by the association of cohesins along the length of sister chromatid arms. In contrast, centromeric cohesin generates intrastrand cohesion and sister centromeres, while highly cohesin enriched, are separated by >800 nm at metaphase in yeast. Removal of cohesin is necessary for sister chromatid separation during anaphase, and this is regulated by evolutionarily conserved polo-like kinase (Cdc5 in yeast, Plk1 in humans). Here we address how high levels of cohesins at centromeric chromatin are removed. Cdc5 associates with centromeric chromatin and cohesin-associated regions. Maximum enrichment of Cdc5 in centromeric chromatin occurs during the metaphase-to-anaphase transition and coincides with the removal of chromosome-associated cohesin. Cdc5 interacts with cohesin in vivo, and cohesin is required for association of Cdc5 at centromeric chromatin. Cohesin removal from centromeric chromatin requires Cdc5 but removal at distal chromosomal arm sites does not. Our results define a novel role for Cdc5 in regulating removal of centromeric cohesins and faithful chromosome segregation.

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2

Daban, Joan-Ramon. "The energy components of stacked chromatin layers explain the morphology, dimensions and mechanical properties of metaphase chromosomes." Journal of The Royal Society Interface 11, no. 92 (March 6, 2014): 20131043. http://dx.doi.org/10.1098/rsif.2013.1043.

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The measurement of the dimensions of metaphase chromosomes in different animal and plant karyotypes prepared in different laboratories indicates that chromatids have a great variety of sizes which are dependent on the amount of DNA that they contain. However, all chromatids are elongated cylinders that have relatively similar shape proportions (length to diameter ratio approx. 13). To explain this geometry, it is considered that chromosomes are self-organizing structures formed by stacked layers of planar chromatin and that the energy of nucleosome–nucleosome interactions between chromatin layers inside the chromatid is approximately 3.6 × 10 −20 J per nucleosome, which is the value reported by other authors for internucleosome interactions in chromatin fibres. Nucleosomes in the periphery of the chromatid are in contact with the medium; they cannot fully interact with bulk chromatin within layers and this generates a surface potential that destabilizes the structure. Chromatids are smooth cylinders because this morphology has a lower surface energy than structures having irregular surfaces. The elongated shape of chromatids can be explained if the destabilizing surface potential is higher in the telomeres (approx. 0.16 mJ m −2 ) than in the lateral surface (approx. 0.012 mJ m −2 ). The results obtained by other authors in experimental studies of chromosome mechanics have been used to test the proposed supramolecular structure. It is demonstrated quantitatively that internucleosome interactions between chromatin layers can justify the work required for elastic chromosome stretching (approx. 0.1 pJ for large chromosomes). The high amount of work (up to approx. 10 pJ) required for large chromosome extensions is probably absorbed by chromatin layers through a mechanism involving nucleosome unwrapping.

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3

Chen, Yu-Fan, Chia-Ching Chou, and Marc R. Gartenberg. "Determinants of Sir2-Mediated, Silent Chromatin Cohesion." Molecular and Cellular Biology 36, no. 15 (May 16, 2016): 2039–50. http://dx.doi.org/10.1128/mcb.00057-16.

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Cohesin associates with distinct sites on chromosomes to mediate sister chromatid cohesion. Single cohesin complexes are thought to bind by encircling both sister chromatids in a topological embrace. Transcriptionally repressed chromosomal domains in the yeastSaccharomyces cerevisiaerepresent specialized sites of cohesion where cohesin binds silent chromatin in a Sir2-dependent fashion. In this study, we investigated the molecular basis for Sir2-mediated cohesion. We identified a cluster of charged surface residues of Sir2, collectively termed the EKDK motif, that are required for cohesin function. In addition, we demonstrated that Esc8, a Sir2-interacting factor, is also required for silent chromatin cohesion. Esc8 was previously shown to associate with Isw1, the enzymatic core of ISW1 chromatin remodelers, to form a variant of the ISW1a chromatin remodeling complex. WhenESC8was deleted or the EKDK motif was mutated, cohesin binding at silenced chromatin domains persisted but cohesion of the domains was abolished. The data are not consistent with cohesin embracing both sister chromatids within silent chromatin domains. Transcriptional silencing remains largely intact in strains lackingESC8or bearing EKDK mutations, indicating that silencing and cohesion are separable functions of Sir2 and silent chromatin.

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4

Giménez-Abián, J. F., D. J. Clarke, A. M. Mullinger, C. S. Downes, and R. T. Johnson. "A postprophase topoisomerase II-dependent chromatid core separation step in the formation of metaphase chromosomes." Journal of Cell Biology 131, no. 1 (October 1, 1995): 7–17. http://dx.doi.org/10.1083/jcb.131.1.7.

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Metaphase chromatids are believed to consist of loops of chromatin anchored to a central scaffold, of which a major component is the decatenatory enzyme DNA topoisomerase II. Silver impregnation selectively stains an axial element of metaphase and anaphase chromatids; but we find that in earlier stages of mitosis, silver staining reveals an initially single, folded midline structure, which separates at prometaphase to form two chromatid axes. Inhibition of topoisomerase II prevents this separation, and also prevents the contraction of chromatids that occurs when metaphase is arrested. Immunolocalization of topoisomerase II alpha reveals chromatid cores analogous to those seen with silver staining. We conclude that the chromatid cores in early mitosis form a single structure, constrained by DNA catenations, which must separate before metaphase chromatids can be resolved.

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5

Muñoz, Sofía, Francesca Passarelli, and Frank Uhlmann. "Conserved roles of chromatin remodellers in cohesin loading onto chromatin." Current Genetics 66, no. 5 (April 10, 2020): 951–56. http://dx.doi.org/10.1007/s00294-020-01075-x.

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Abstract Cohesin is a conserved, ring-shaped protein complex that topologically entraps DNA. This ability makes this member of the structural maintenance of chromosomes (SMC) complex family a central hub of chromosome dynamics regulation. Besides its essential role in sister chromatid cohesion, cohesin shapes the interphase chromatin domain architecture and plays important roles in transcriptional regulation and DNA repair. Cohesin is loaded onto chromosomes at centromeres, at the promoters of highly expressed genes, as well as at DNA replication forks and sites of DNA damage. However, the features that determine these binding sites are still incompletely understood. We recently described a role of the budding yeast RSC chromatin remodeler in cohesin loading onto chromosomes. RSC has a dual function, both as a physical chromatin receptor of the Scc2/Scc4 cohesin loader complex, as well as by providing a nucleosome-free template for cohesin loading. Here, we show that the role of RSC in sister chromatid cohesion is conserved in fission yeast. We discuss what is known about the broader conservation of the contribution of chromatin remodelers to cohesin loading onto chromatin.

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6

Stephens, Andrew D., Julian Haase, Leandra Vicci, Russell M. Taylor, and Kerry Bloom. "Cohesin, condensin, and the intramolecular centromere loop together generate the mitotic chromatin spring." Journal of Cell Biology 193, no. 7 (June 27, 2011): 1167–80. http://dx.doi.org/10.1083/jcb.201103138.

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Sister chromatid cohesion provides the mechanistic basis, together with spindle microtubules, for generating tension between bioriented chromosomes in metaphase. Pericentric chromatin forms an intramolecular loop that protrudes bidirectionally from the sister chromatid axis. The centromere lies on the surface of the chromosome at the apex of each loop. The cohesin and condensin structural maintenance of chromosomes (SMC) protein complexes are concentrated within the pericentric chromatin, but whether they contribute to tension-generating mechanisms is not known. To understand how pericentric chromatin is packaged and resists tension, we map the position of cohesin (SMC3), condensin (SMC4), and pericentric LacO arrays within the spindle. Condensin lies proximal to the spindle axis and is responsible for axial compaction of pericentric chromatin. Cohesin is radially displaced from the spindle axis and confines pericentric chromatin. Pericentric cohesin and condensin contribute to spindle length regulation and dynamics in metaphase. Together with the intramolecular centromere loop, these SMC complexes constitute a molecular spring that balances spindle microtubule force in metaphase.

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7

SIMPSON, R. T. "Chromatin Research Surveyed: Chromatin." Science 243, no. 4895 (March 3, 1989): 1220. http://dx.doi.org/10.1126/science.243.4895.1220.

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8

Lawrimore, Josh, Ayush Doshi, Brandon Friedman, Elaine Yeh, and Kerry Bloom. "Geometric partitioning of cohesin and condensin is a consequence of chromatin loops." Molecular Biology of the Cell 29, no. 22 (November 2018): 2737–50. http://dx.doi.org/10.1091/mbc.e18-02-0131.

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SMC (structural maintenance of chromosomes) complexes condensin and cohesin are crucial for proper chromosome organization. Condensin has been reported to be a mechanochemical motor capable of forming chromatin loops, while cohesin passively diffuses along chromatin to tether sister chromatids. In budding yeast, the pericentric region is enriched in both condensin and cohesin. As in higher-eukaryotic chromosomes, condensin is localized to the axial chromatin of the pericentric region, while cohesin is enriched in the radial chromatin. Thus, the pericentric region serves as an ideal model for deducing the role of SMC complexes in chromosome organization. We find condensin-mediated chromatin loops establish a robust chromatin organization, while cohesin limits the area that chromatin loops can explore. Upon biorientation, extensional force from the mitotic spindle aggregates condensin-bound chromatin from its equilibrium position to the axial core of pericentric chromatin, resulting in amplified axial tension. The axial localization of condensin depends on condensin’s ability to bind to chromatin to form loops, while the radial localization of cohesin depends on cohesin’s ability to diffuse along chromatin. The different chromatin-tethering modalities of condensin and cohesin result in their geometric partitioning in the presence of an extensional force on chromatin.

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9

Ghaddar, Nagham, Pierre Luciano, Vincent Géli, and Yves Corda. "Chromatin assembly factor-1 preserves genome stability in ctf4∆ cells by promoting sister chromatid cohesion." Cell Stress 7, no. 9 (September 11, 2023): 69–89. http://dx.doi.org/10.15698/cst2023.09.289.

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Chromatin assembly and the establishment of sister chromatid cohesion are intimately connected to the progression of DNA replication forks. Here we examined the genetic interaction between the heterotrimeric chromatin assembly factor-1 (CAF-1), a central component of chromatin assembly during replication, and the core replisome component Ctf4. We find that CAF-1 deficient cells as well as cells affected in newly-synthesized H3-H4 histones deposition during DNA replication exhibit a severe negative growth with ctf4∆ mutant. We dissected the role of CAF-1 in the maintenance of genome stability in ctf4∆ yeast cells. In the absence of CTF4, CAF-1 is essential for viability in cells experiencing replication problems, in cells lacking functional S-phase checkpoint or functional spindle checkpoint, and in cells lacking DNA repair pathways involving homologous recombination. We present evidence that CAF-1 affects cohesin association to chromatin in a DNA-damage-dependent manner and is essential to maintain cohesion in the absence of CTF4. We also show that Eco1-catalyzed Smc3 acetylation is reduced in absence of CAF-1. Furthermore, we describe genetic interactions between CAF-1 and essential genes involved in cohesin loading, cohesin stabilization, and cohesin component indicating that CAF-1 is crucial for viability when sister chromatid cohesion is affected. Finally, our data indicate that the CAF-1-dependent pathway required for cohesion is functionally distinct from the Rtt101-Mms1-Mms22 pathway which functions in replicated chromatin assembly. Collectively, our results suggest that the deposition by CAF-1 of newly-synthesized H3-H4 histones during DNA replication creates a chromatin environment that favors sister chromatid cohesion and maintains genome integrity.

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10

Stanyte, Rugile, Johannes Nuebler, Claudia Blaukopf, Rudolf Hoefler, Roman Stocsits, Jan-Michael Peters, and Daniel W. Gerlich. "Dynamics of sister chromatid resolution during cell cycle progression." Journal of Cell Biology 217, no. 6 (April 25, 2018): 1985–2004. http://dx.doi.org/10.1083/jcb.201801157.

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Faithful genome transmission in dividing cells requires that the two copies of each chromosome’s DNA package into separate but physically linked sister chromatids. The linkage between sister chromatids is mediated by cohesin, yet where sister chromatids are linked and how they resolve during cell cycle progression has remained unclear. In this study, we investigated sister chromatid organization in live human cells using dCas9-mEGFP labeling of endogenous genomic loci. We detected substantial sister locus separation during G2 phase irrespective of the proximity to cohesin enrichment sites. Almost all sister loci separated within a few hours after their respective replication and then rapidly equilibrated their average distances within dynamic chromatin polymers. Our findings explain why the topology of sister chromatid resolution in G2 largely reflects the DNA replication program. Furthermore, these data suggest that cohesin enrichment sites are not persistent cohesive sites in human cells. Rather, cohesion might occur at variable genomic positions within the cell population.

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11

Gallego-Paez, Lina Marcela, Hiroshi Tanaka, Masashige Bando, Motoko Takahashi, Naohito Nozaki, Ryuichiro Nakato, Katsuhiko Shirahige, and Toru Hirota. "Smc5/6-mediated regulation of replication progression contributes to chromosome assembly during mitosis in human cells." Molecular Biology of the Cell 25, no. 2 (January 15, 2014): 302–17. http://dx.doi.org/10.1091/mbc.e13-01-0020.

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The structural maintenance of chromosomes (SMC) proteins constitute the core of critical complexes involved in structural organization of chromosomes. In yeast, the Smc5/6 complex is known to mediate repair of DNA breaks and replication of repetitive genomic regions, including ribosomal DNA loci and telomeres. In mammalian cells, which have diverse genome structure and scale from yeast, the Smc5/6 complex has also been implicated in DNA damage response, but its further function in unchallenged conditions remains elusive. In this study, we addressed the behavior and function of Smc5/6 during the cell cycle. Chromatin fractionation, immunofluorescence, and live-cell imaging analyses indicated that Smc5/6 associates with chromatin during interphase but largely dissociates from chromosomes when they condense in mitosis. Depletion of Smc5 and Smc6 resulted in aberrant mitotic chromosome phenotypes that were accompanied by the abnormal distribution of topoisomerase IIα (topo IIα) and condensins and by chromosome segregation errors. Importantly, interphase chromatin structure indicated by the premature chromosome condensation assay suggested that Smc5/6 is required for the on-time progression of DNA replication and subsequent binding of topo IIα on replicated chromatids. These results indicate an essential role of the Smc5/6 complex in processing DNA replication, which becomes indispensable for proper sister chromatid assembly in mitosis.

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12

Novak, Ivana, Hong Wang, Ekaterina Revenkova, Rolf Jessberger, Harry Scherthan, and Christer Höög. "Cohesin Smc1β determines meiotic chromatin axis loop organization." Journal of Cell Biology 180, no. 1 (January 7, 2008): 83–90. http://dx.doi.org/10.1083/jcb.200706136.

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Meiotic chromosomes consist of proteinaceous axial structures from which chromatin loops emerge. Although we know that loop density along the meiotic chromosome axis is conserved in organisms with different genome sizes, the basis for the regular spacing of chromatin loops and their organization is largely unknown. We use two mouse model systems in which the postreplicative meiotic chromosome axes in the mutant oocytes are either longer or shorter than in wild-type oocytes. We observe a strict correlation between chromosome axis extension and a general and reciprocal shortening of chromatin loop size. However, in oocytes with a shorter chromosome axis, only a subset of the chromatin loops is extended. We find that the changes in chromatin loop size observed in oocytes with shorter or longer chromosome axes depend on the structural maintenance of chromosomes 1β (Smc1β), a mammalian chromosome–associated meiosis-specific cohesin. Our results suggest that in addition to its role in sister chromatid cohesion, Smc1β determines meiotic chromatin loop organization.

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13

FELSENFELD, G., B. BURGESS-BEUSSE, C. FARRELL, M. GASZNER, R. GHIRLANDO, S. HUANG, C. JIN, et al. "Chromatin Boundaries and Chromatin Domains." Cold Spring Harbor Symposia on Quantitative Biology 69 (January 1, 2004): 245–50. http://dx.doi.org/10.1101/sqb.2004.69.245.

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14

Palmateer, Colleen M., Shawn C. Moseley, Surjyendu Ray, Savannah G. Brovero, and Michelle N. Arbeitman. "Analysis of cell-type-specific chromatin modifications and gene expression in Drosophila neurons that direct reproductive behavior." PLOS Genetics 17, no. 4 (April 26, 2021): e1009240. http://dx.doi.org/10.1371/journal.pgen.1009240.

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Examining the role of chromatin modifications and gene expression in neurons is critical for understanding how the potential for behaviors are established and maintained. We investigate this question by examining Drosophila melanogaster fru P1 neurons that underlie reproductive behaviors in both sexes. We developed a method to purify cell-type-specific chromatin (Chromatag), using a tagged histone H2B variant that is expressed using the versatile Gal4/UAS gene expression system. Here, we use Chromatag to evaluate five chromatin modifications, at three life stages in both sexes. We find substantial changes in chromatin modification profiles across development and fewer differences between males and females. Additionally, we find chromatin modifications that persist in different sets of genes from pupal to adult stages, which may point to genes important for cell fate determination in fru P1 neurons. We generated cell-type-specific RNA-seq data sets, using translating ribosome affinity purification (TRAP). We identify actively translated genes in fru P1 neurons, revealing novel stage- and sex-differences in gene expression. We also find chromatin modification enrichment patterns that are associated with gene expression. Next, we use the chromatin modification data to identify cell-type-specific super-enhancer-containing genes. We show that genes with super-enhancers in fru P1 neurons differ across development and between the sexes. We validated that a set of genes are expressed in fru P1 neurons, which were chosen based on having a super-enhancer and TRAP-enriched expression in fru P1 neurons.

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Sapkota, Hem, Emilia Wasiak, John R. Daum, and Gary J. Gorbsky. "Multiple determinants and consequences of cohesion fatigue in mammalian cells." Molecular Biology of the Cell 29, no. 15 (August 2018): 1811–24. http://dx.doi.org/10.1091/mbc.e18-05-0315.

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Cells delayed in metaphase with intact mitotic spindles undergo cohesion fatigue, where sister chromatids separate asynchronously, while cells remain in mitosis. Cohesion fatigue requires release of sister chromatid cohesion. However, the pathways that breach sister chromatid cohesion during cohesion fatigue remain unknown. Using moderate-salt buffers to remove loosely bound chromatin cohesin, we show that “cohesive” cohesin is not released during chromatid separation during cohesion fatigue. Using a regulated protein heterodimerization system to lock different cohesin ring interfaces at specific times in mitosis, we show that the Wapl-mediated pathway of cohesin release is not required for cohesion fatigue. By manipulating microtubule stability and cohesin complex integrity in cell lines with varying sensitivity to cohesion fatigue, we show that rates of cohesion fatigue reflect a dynamic balance between spindle pulling forces and resistance to separation by interchromatid cohesion. Finally, while massive separation of chromatids in cohesion fatigue likely produces inviable cell progeny, we find that short metaphase delays, leading to partial chromatid separation, predispose cells to chromosome missegregation. Thus, complete separation of one or a few chromosomes and/or partial separation of sister chromatids may be an unrecognized but common source of chromosome instability that perpetuates the evolution of malignant cells in cancer.

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Cimini, Daniela, Marta Mattiuzzo, Liliana Torosantucci, and Francesca Degrassi. "Histone Hyperacetylation in Mitosis Prevents Sister Chromatid Separation and Produces Chromosome Segregation Defects." Molecular Biology of the Cell 14, no. 9 (September 2003): 3821–33. http://dx.doi.org/10.1091/mbc.e03-01-0860.

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Posttranslational modifications of core histones contribute to driving changes in chromatin conformation and compaction. Herein, we investigated the role of histone deacetylation on the mitotic process by inhibiting histone deacetylases shortly before mitosis in human primary fibroblasts. Cells entering mitosis with hyperacetylated histones displayed altered chromatin conformation associated with decreased reactivity to the anti-Ser 10 phospho H3 antibody, increased recruitment of protein phosphatase 1-δ on mitotic chromosomes, and depletion of heterochromatin protein 1 from the centromeric heterochromatin. Inhibition of histone deacetylation before mitosis produced defective chromosome condensation and impaired mitotic progression in living cells, suggesting that improper chromosome condensation may induce mitotic checkpoint activation. In situ hybridization analysis on anaphase cells demonstrated the presence of chromatin bridges, which were caused by persisting cohesion along sister chromatid arms after centromere separation. Thus, the presence of hyperacetylated chromatin during mitosis impairs proper chromosome condensation during the pre-anaphase stages, resulting in poor sister chromatid resolution. Lagging chromosomes consisting of single or paired sisters were also induced by the presence of hyperacetylated histones, indicating that the less constrained centromeric organization associated with heterochromatin protein 1 depletion may promote the attachment of kinetochores to microtubules coming from both poles.

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17

Riedel, Christian G., Juraj Gregan, Stephan Gruber, and Kim Nasmyth. "Is chromatin remodeling required to build sister-chromatid cohesion?" Trends in Biochemical Sciences 29, no. 8 (August 2004): 389–92. http://dx.doi.org/10.1016/j.tibs.2004.06.007.

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18

Urnov, Fyodor, and Colyn Crane-Robinson. "Chromatin." European Journal of Biochemistry 269, no. 9 (May 2002): 2267. http://dx.doi.org/10.1046/j.1432-1033.2002.02884.x.

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19

Gross, David S., Surabhi Chowdhary, Jayamani Anandhakumar, and Amoldeep S. Kainth. "Chromatin." Current Biology 25, no. 24 (December 2015): R1158—R1163. http://dx.doi.org/10.1016/j.cub.2015.10.059.

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20

Gross, David S., Surabhi Chowdhary, Jayamani Anandhakumar, and Amoldeep S. Kainth. "Chromatin." Current Biology 26, no. 4 (February 2016): 556. http://dx.doi.org/10.1016/j.cub.2016.02.002.

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21

Langmore, John P. "Chromatin." Cell 59, no. 2 (October 1989): 243–44. http://dx.doi.org/10.1016/0092-8674(89)90284-5.

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22

Racko, Dusan, Fabrizio Benedetti, Dimos Goundaroulis, and Andrzej Stasiak. "Chromatin Loop Extrusion and Chromatin Unknotting." Polymers 10, no. 10 (October 11, 2018): 1126. http://dx.doi.org/10.3390/polym10101126.

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It has been a puzzle how decondensed interphase chromosomes remain essentially unknotted. The natural expectation is that in the presence of type II DNA topoisomerases that permit passages of double-stranded DNA regions through each other, all chromosomes should reach the state of topological equilibrium. The topological equilibrium in highly crowded interphase chromosomes forming chromosome territories would result in formation of highly knotted chromatin fibres. However, Chromosome Conformation Capture (3C) methods revealed that the decay of contact probabilities with the genomic distance in interphase chromosomes is practically the same as in the crumpled globule state that is formed when long polymers condense without formation of any knots. To remove knots from highly crowded chromatin, one would need an active process that should not only provide the energy to move the system from the state of topological equilibrium but also guide topoisomerase-mediated passages in such a way that knots would be efficiently unknotted instead of making the knots even more complex. We perform coarse-grained molecular dynamics simulations of the process of chromatin loop extrusion involving knotted and catenated chromatin fibres to check whether chromatin loop extrusion may be involved in active unknotting of chromatin fibres. Our simulations show that the process of chromatin loop extrusion is ideally suited to actively unknot, decatenate and demix chromatin fibres in interphase chromosomes.

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Mello, MLS, AS Moraes, and BC Vidal. "Extended chromatin fibers and chromatin organization." Biotechnic & Histochemistry 86, no. 4 (January 28, 2010): 213–25. http://dx.doi.org/10.3109/10520290903549022.

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24

Stephens, Andrew D., Rachel A. Haggerty, Paula A. Vasquez, Leandra Vicci, Chloe E. Snider, Fu Shi, Cory Quammen, et al. "Pericentric chromatin loops function as a nonlinear spring in mitotic force balance." Journal of Cell Biology 200, no. 6 (March 18, 2013): 757–72. http://dx.doi.org/10.1083/jcb.201208163.

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The mechanisms by which sister chromatids maintain biorientation on the metaphase spindle are critical to the fidelity of chromosome segregation. Active force interplay exists between predominantly extensional microtubule-based spindle forces and restoring forces from chromatin. These forces regulate tension at the kinetochore that silences the spindle assembly checkpoint to ensure faithful chromosome segregation. Depletion of pericentric cohesin or condensin has been shown to increase the mean and variance of spindle length, which have been attributed to a softening of the linear chromatin spring. Models of the spindle apparatus with linear chromatin springs that match spindle dynamics fail to predict the behavior of pericentromeric chromatin in wild-type and mutant spindles. We demonstrate that a nonlinear spring with a threshold extension to switch between spring states predicts asymmetric chromatin stretching observed in vivo. The addition of cross-links between adjacent springs recapitulates coordination between pericentromeres of neighboring chromosomes.

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25

Ishak, Muhiddin, Rashidah Baharudin, Isa Mohamed Rose, Ismail Sagap, Luqman Mazlan, Zairul Azwan Mohd Azman, Nadiah Abu, Rahman Jamal, Learn-Han Lee, and Nurul Syakima Ab Mutalib. "Genome-Wide Open Chromatin Methylome Profiles in Colorectal Cancer." Biomolecules 10, no. 5 (May 5, 2020): 719. http://dx.doi.org/10.3390/biom10050719.

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The methylome of open chromatins was investigated in colorectal cancer (CRC) to explore cancer-specific methylation and potential biomarkers. Epigenome-wide methylome of open chromatins was studied in colorectal cancer tissues using the Infinium DNA MethylationEPIC assay. Differentially methylated regions were identified using the ChAMP Bioconductor. Our stringent analysis led to the discovery of 2187 significant differentially methylated open chromatins in CRCs. More hypomethylated probes were observed and the trend was similar across all chromosomes. The majority of hyper- and hypomethylated probes in open chromatin were in chromosome 1. Our unsupervised hierarchical clustering analysis showed that 40 significant differentially methylated open chromatins were able to segregate CRC from normal colonic tissues. Receiver operating characteristic analyses from the top 40 probes revealed several significant, highly discriminative, specific and sensitive probes such as OPLAH cg26256223, EYA4 cg01328892, and CCNA1 cg11513637, among others. OPLAH cg26256223 hypermethylation is associated with reduced gene expression in the CRC. This study reports many open chromatin loci with novel differential methylation statuses, some of which with the potential as candidate markers for diagnostic purposes.

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Green, G. R., R. R. Ferlita, W. F. Walkenhorst, and D. L. Poccia. "Linker DNA destabilizes condensed chromatin." Biochemistry and Cell Biology 79, no. 3 (June 1, 2001): 349–63. http://dx.doi.org/10.1139/o01-115.

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The contribution of the linker region to maintenance of condensed chromatin was examined in two model systems, namely sea urchin sperm nuclei and chicken red blood cell nuclei. Linkerless nuclei, prepared by extensive digestion with micrococcal nuclease, were compared with Native nuclei using several assays, including microscopic appearance, nuclear turbidity, salt stability, and trypsin resistance. Chromatin in the Linkerless nuclei was highly condensed, resembling pyknotic chromatin in apoptotic cells. Linkerless nuclei were more stable in low ionic strength buffers and more resistant to trypsin than Native nuclei. Analysis of histones from the trypsinized nuclei by polyacrylamide gel electrophoresis showed that specific histone H1, H2B, and H3 tail regions stabilized linker DNA in condensed nuclei. Thermal denaturation of soluble chromatin preparations from differentially trypsinized sperm nuclei demonstrated that the N-terminal regions of histones Sp H1, Sp H2B, and H3 bind tightly to linker DNA, causing it to denature at a high temperature. We conclude that linker DNA exerts a disruptive force on condensed chromatin structure which is counteracted by binding of specific histone tail regions to the linker DNA. The inherent instability of the linker region may be significant in all eukaryotic chromatins and may promote gene activation in living cells.Key words: chromatin condensation, sea urchin sperm, chicken red blood cell, nuclei, linker DNA, histone variants, micrococcal nuclease, nucleosome, trypsin, gel electrophoresis.

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27

Samejima, Kumiko, Itaru Samejima, Paola Vagnarelli, Hiromi Ogawa, Giulia Vargiu, David A. Kelly, Flavia de Lima Alves, et al. "Mitotic chromosomes are compacted laterally by KIF4 and condensin and axially by topoisomerase IIα." Journal of Cell Biology 199, no. 5 (November 19, 2012): 755–70. http://dx.doi.org/10.1083/jcb.201202155.

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Mitotic chromosome formation involves a relatively minor condensation of the chromatin volume coupled with a dramatic reorganization into the characteristic “X” shape. Here we report results of a detailed morphological analysis, which revealed that chromokinesin KIF4 cooperated in a parallel pathway with condensin complexes to promote the lateral compaction of chromatid arms. In this analysis, KIF4 and condensin were mutually dependent for their dynamic localization on the chromatid axes. Depletion of either caused sister chromatids to expand and compromised the “intrinsic structure” of the chromosomes (defined in an in vitro assay), with loss of condensin showing stronger effects. Simultaneous depletion of KIF4 and condensin caused complete loss of chromosome morphology. In these experiments, topoisomerase IIα contributed to shaping mitotic chromosomes by promoting the shortening of the chromatid axes and apparently acting in opposition to the actions of KIF4 and condensins. These three proteins are major determinants in shaping the characteristic mitotic chromosome morphology.

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Krieger, Lisa Marie, Emil Mladenov, Aashish Soni, Marilen Demond, Martin Stuschke, and George Iliakis. "Disruption of Chromatin Dynamics by Hypotonic Stress Suppresses HR and Shifts DSB Processing to Error-Prone SSA." International Journal of Molecular Sciences 22, no. 20 (October 11, 2021): 10957. http://dx.doi.org/10.3390/ijms222010957.

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The processing of DNA double-strand breaks (DSBs) depends on the dynamic characteristics of chromatin. To investigate how abrupt changes in chromatin compaction alter these dynamics and affect DSB processing and repair, we exposed irradiated cells to hypotonic stress (HypoS). Densitometric and chromosome-length analyses show that HypoS transiently decompacts chromatin without inducing histone modifications known from regulated local chromatin decondensation, or changes in Micrococcal Nuclease (MNase) sensitivity. HypoS leaves undisturbed initial stages of DNA-damage-response (DDR), such as radiation-induced ATM activation and H2AX-phosphorylation. However, detection of ATM-pS1981, γ-H2AX and 53BP1 foci is reduced in a protein, cell cycle phase and cell line dependent manner; likely secondary to chromatin decompaction that disrupts the focal organization of DDR proteins. While HypoS only exerts small effects on classical nonhomologous end-joining (c-NHEJ) and alternative end-joining (alt-EJ), it markedly suppresses homologous recombination (HR) without affecting DNA end-resection at DSBs, and clearly enhances single-strand annealing (SSA). These shifts in pathway engagement are accompanied by decreases in HR-dependent chromatid-break repair in the G2-phase, and by increases in alt-EJ and SSA-dependent chromosomal translocations. Consequently, HypoS sensitizes cells to ionizing radiation (IR)-induced killing. We conclude that HypoS-induced global chromatin decompaction compromises regulated chromatin dynamics and genomic stability by suppressing DSB-processing by HR, and allowing error-prone processing by alt-EJ and SSA.

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29

Min, Sunwoo, Ho-Soo Lee, Jae-Hoon Ji, Yungyeong Heo, Yonghyeon Kim, Sunyoung Chae, Yong Won Choi, Ho-Chul Kang, Makoto Nakanishi, and Hyeseong Cho. "The chromatin remodeler RSF1 coordinates epigenetic marks for transcriptional repression and DSB repair." Nucleic Acids Research 49, no. 21 (November 25, 2021): 12268–83. http://dx.doi.org/10.1093/nar/gkab1093.

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Abstract DNA lesions impact on local transcription and the damage-induced transcriptional repression facilitates efficient DNA repair. However, how chromatin dynamics cooperates with these two events remained largely unknown. We here show that histone H2A acetylation at K118 is enriched in transcriptionally active regions. Under DNA damage, the RSF1 chromatin remodeling factor recruits HDAC1 to DSB sites. The RSF1-HDAC1 complex induces the deacetylation of H2A(X)-K118 and its deacetylation is indispensable for the ubiquitination of histone H2A at K119. Accordingly, the acetylation mimetic H2A-K118Q suppressed the H2A-K119ub level, perturbing the transcriptional repression at DNA lesions. Intriguingly, deacetylation of H2AX at K118 also licenses the propagation of γH2AX and recruitment of MDC1. Consequently, the H2AX-K118Q limits DNA repair. Together, the RSF1-HDAC1 complex controls the traffic of the DNA damage response and transcription simultaneously in transcriptionally active chromatins. The interplay between chromatin remodelers and histone modifiers highlights the importance of chromatin versatility in the maintenance of genome integrity.

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30

Sinclair, Paul, Qian Bian, Matt Plutz, Edith Heard, and Andrew S. Belmont. "Dynamic plasticity of large-scale chromatin structure revealed by self-assembly of engineered chromosome regions." Journal of Cell Biology 190, no. 5 (September 6, 2010): 761–76. http://dx.doi.org/10.1083/jcb.200912167.

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Interphase chromatin compaction well above the 30-nm fiber is well documented, but the structural motifs underlying this level of chromatin folding remain unknown. Taking a reductionist approach, we analyzed in mouse embryonic stem (ES) cells and ES-derived fibroblasts and erythroblasts the folding of 10–160-megabase pair engineered chromosome regions consisting of tandem repeats of bacterial artificial chromosomes (BACs) containing ∼200 kilobases of mammalian genomic DNA tagged with lac operator (LacO) arrays. Unexpectedly, linear mitotic and interphase chromatid regions formed from noncontiguously folded DNA topologies. Particularly, in ES cells, these model chromosome regions self-organized with distant sequences segregating into functionally distinct, compact domains. Transcriptionally active and histone H3K27me3-modified regions positioned toward the engineered chromosome subterritory exterior, with LacO repeats and the BAC vector backbone localizing within an H3K9me3, HP1-enriched core. Differential compaction of Dhfr and α- and β-globin transgenes was superimposed on dramatic, lineage-specific reorganization of large-scale chromatin folding, demonstrating a surprising plasticity of large-scale chromatin organization.

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31

Hendzel, Michael J., Michael J. Kruhlak, and David P. Bazett-Jones. "Organization of Highly Acetylated Chromatin around Sites of Heterogeneous Nuclear RNA Accumulation." Molecular Biology of the Cell 9, no. 9 (September 1998): 2491–507. http://dx.doi.org/10.1091/mbc.9.9.2491.

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Histones found within transcriptionally competent and active regions of the genome are highly acetylated. Moreover, these highly acetylated histones have very short half-lives. Thus, both histone acetyltransferases and histone deacetylases must enrich within or near these euchromatic regions of the interphase chromatids. Using an antibody specific for highly acetylated histone H3, we have investigated the organization of transcriptionally active and competent chromatin as well as nuclear histone acetyltransferase and deacetylase activities. We observe an exclusion of highly acetylated chromatin around the periphery of the nucleus and an enrichment near interchromatin granule clusters (IGCs). The highly acetylated chromatin is found in foci that may reflect the organization of highly acetylated chromatin into “chromonema” fibers. Transmission electron microscopy of Indian muntjac fibroblast cell nuclei indicates that the chromatin associated with the periphery of IGCs remains relatively condensed, most commonly found in domains containing chromatin folded beyond 30 nm. Using electron spectroscopic imaging, we demonstrate that IGCs are clusters of ribonucleoprotein particles. The individual granules comprise RNA-rich fibrils or globular regions that fold into individual granules. Quantitative analysis of individual granules indicates that they contain variable amounts of RNA estimated between 1.5 and >10 kb. We propose that interchromatin granules are heterogeneous nuclear RNA-containing particles, some of which may be pre-mRNA generated by nearby transcribed chromatin. An intermediary zone between the IGC and surrounding chromatin is described that contains factors with the potential to provide specificity to the localization of sequences near IGCs.

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32

Hiraoka, Yasushi. "Chromatin Unlimited: An Evolutionary View of Chromatin." Epigenomes 6, no. 1 (January 2, 2022): 2. http://dx.doi.org/10.3390/epigenomes6010002.

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33

Ogiwara, Hideaki, Takemi Enomoto, and Masayuki Seki. "The INO80 Chromatin Remodeling Complex Functions in Sister Chromatid Cohesion." Cell Cycle 6, no. 9 (May 2, 2007): 1090–95. http://dx.doi.org/10.4161/cc.6.9.4130.

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34

Korfanty, Joanna, Tomasz Stokowy, Marek Chadalski, Agnieszka Toma-Jonik, Natalia Vydra, Piotr Widłak, Bartosz Wojtaś, Bartłomiej Gielniewski, and Wieslawa Widlak. "SPEN protein expression and interactions with chromatin in mouse testicular cells." Reproduction 156, no. 3 (September 2018): 195–206. http://dx.doi.org/10.1530/rep-18-0046.

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SPEN (spen family transcription repressor) is a nucleic acid-binding protein putatively involved in repression of gene expression. We hypothesized that SPEN could be involved in general downregulation of the transcription during the heat shock response in mouse spermatogenic cells through its interactions with chromatin. We documented predominant nuclear localization of the SPEN protein in spermatocytes and round spermatids, which was retained after heat shock. Moreover, the protein was excluded from the highly condensed chromatin. Chromatin immunoprecipitation experiments clearly indicated interactions of SPEN with chromatinin vivo. However, ChIP-Seq analyses did not reveal any strong specific peaks both in untreated and heat shocked cells, which might suggest dispersed localization of SPEN and/or its indirect binding to DNA. Usingin situproximity ligation assay we found closein vivoassociations of SPEN with MTA1 (metastasis-associated 1), a member of the nucleosome remodeling complex with histone deacetylase activity, which might contribute to interactions of SPEN with chromatin.

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35

Ehrensberger, Andreas Hasso, and Jesper Qualmann Svejstrup. "Reprogramming chromatin." Critical Reviews in Biochemistry and Molecular Biology 47, no. 5 (July 3, 2012): 464–82. http://dx.doi.org/10.3109/10409238.2012.697125.

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36

Schulze, Julia M., Alice Y. Wang, and Michael S. Kobor. "Reading chromatin." Epigenetics 5, no. 7 (October 2010): 573–77. http://dx.doi.org/10.4161/epi.5.7.12856.

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37

Black, Joshua C., and Johnathan R. Whetstine. "Chromatin landscape." Epigenetics 6, no. 1 (January 2011): 9–15. http://dx.doi.org/10.4161/epi.6.1.13331.

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38

G. Fuentes-Mascorro, H. Serrano, A. "SPERM CHROMATIN." Archives of Andrology 45, no. 3 (January 2000): 215–25. http://dx.doi.org/10.1080/01485010050193995.

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39

Kornberg, Roger D., and Yahli Lorch. "Chromatin rules." Nature Structural & Molecular Biology 14, no. 11 (November 2007): 986–88. http://dx.doi.org/10.1038/nsmb1107-986.

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40

Hübner, Michael R., and David L. Spector. "Chromatin Dynamics." Annual Review of Biophysics 39, no. 1 (April 2010): 471–89. http://dx.doi.org/10.1146/annurev.biophys.093008.131348.

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41

Tuma, Rabiya S. "Chromatin zigzags." Journal of Cell Biology 174, no. 1 (July 3, 2006): 2. http://dx.doi.org/10.1083/jcb.1741iti1.

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42

Tyler, Jessica K. "Chromatin assembly." European Journal of Biochemistry 269, no. 9 (April 22, 2002): 2268–74. http://dx.doi.org/10.1046/j.1432-1033.2002.02890.x.

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43

Watanabe, Shinya, and Craig L. Peterson. "Chromatin dynamics." Cell Cycle 12, no. 15 (August 2013): 2337–38. http://dx.doi.org/10.4161/cc.25704.

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44

Lue, N. F. "Chromatin Remodeling." Science Signaling 2005, no. 294 (July 19, 2005): tr20. http://dx.doi.org/10.1126/stke.2942005tr20.

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45

Recillas-Targa, F. "Chromatin everywhere." Briefings in Functional Genomics 10, no. 1 (January 1, 2011): 1–2. http://dx.doi.org/10.1093/bfgp/elr006.

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46

Babbitt, Gregory. "Chromatin Evolving." American Scientist 99, no. 1 (2011): 48. http://dx.doi.org/10.1511/2011.88.48.

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47

Felsenfeld, Gary. "Chromatin Unfolds." Cell 86, no. 1 (July 1996): 13–19. http://dx.doi.org/10.1016/s0092-8674(00)80073-2.

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48

Lomvardas, Stavros, and Dimitris Thanos. "Opening Chromatin." Molecular Cell 9, no. 2 (February 2002): 209–11. http://dx.doi.org/10.1016/s1097-2765(02)00463-x.

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49

Meyer, Peter. "Chromatin remodelling." Current Opinion in Plant Biology 4, no. 5 (October 2001): 457–62. http://dx.doi.org/10.1016/s1369-5266(00)00200-4.

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Woodcock, Christopher L. "Chromatin architecture." Current Opinion in Structural Biology 16, no. 2 (April 2006): 213–20. http://dx.doi.org/10.1016/j.sbi.2006.02.005.

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