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Journal articles on the topic 'Chromatin-remodelling'

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Published: 4 June 2021
Last updated: 9 March 2023

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1

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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2

Ho, Lena, and Gerald R. Crabtree. "Chromatin remodelling during development." Nature 463, no. 7280 (January 2010): 474–84. http://dx.doi.org/10.1038/nature08911.

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3

Flaus, A., I. Whitehouse, C. Stockdale, K. Havas, M. Bruno, N. Wiechens, and T. A. Owen-Hughes. "Pathways for remodelling chromatin." Biochemical Society Transactions 30, no. 5 (October 1, 2002): A97. http://dx.doi.org/10.1042/bst030a097.

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4

Owen-Hughes, T. "Pathways for remodelling chromatin." Biochemical Society Transactions 31, no. 5 (October 1, 2003): 893–905. http://dx.doi.org/10.1042/bst0310893.

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The alteration of chromatin structure plays an integral role in gene regulation. One means by which eukaryotes manipulate chromatin structure involves the use of ATP-dependent chromatin-remodelling enzymes. It appears likely that these enzymes play a widespread role in the regulation of many nuclear processes. Recently, significant progress has been made in defining the alterations to chromatin structure that these enzymes generate. The ability to alter nucleosome positioning may be a common feature of all ATP-dependent remodelling enzymes, but the spectrum of positions to which nucleosomes are relocated varies. Mounting evidence supports the ability of remodelling enzymes to translocate along DNA. This provides a means by which they could alter both the twist and writhe of DNA on the surface of nucleosomes, and so accelerate nucleosome repositioning.
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5

Willard, Huntington F., and Helen K. Salz. "Remodelling chromatin with RNA." Nature 386, no. 6622 (March 1997): 228–29. http://dx.doi.org/10.1038/386228a0.

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6

Whitehouse, I., A. Flaus, K. Havas, and T. Owen-Hughes. "Mechanisms for ATP-dependent chromatin remodelling." Biochemical Society Transactions 28, no. 4 (August 1, 2000): 376–79. http://dx.doi.org/10.1042/bst0280376.

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Gene regulation involves the generation of a local chromatin topology that is conducive to transcription. Several classes of chromatin remodelling activity have been shown to play a role in this process. ATP-dependent chromatin-remodelling activities use energy derived from the hydrolysis of ATP to alter the structure of chromatin, making it more accessible for transcription factor binding. The yeast SWI-SWF complex is the founding member of this family of ATP-dependent chromatin-remodelling activities. We have developed a model system to study the ability of the SWI-SWF complex to alter chromatin structure. Using this system, we find that SWI-SWF is able to alter the position of nucleosomes along the DNA. This is consistent with recent reports that other ATP-dependent chromatin-remodelling activities can alter the positions of nucleosomes along DNA. This suggests that nucleosome mobilization may be a general feature of the activity of ATP-dependent chromatin-remodelling activities. Some of the mechanisms by which nucleosomes may be moved along DNA are discussed.
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7

Sundaramoorthy, Ramasubramian, and Tom Owen-Hughes. "Chromatin remodelling comes into focus." F1000Research 9 (August 20, 2020): 1011. http://dx.doi.org/10.12688/f1000research.21933.1.

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ATP-dependent chromatin remodelling enzymes are molecular machines that act to reconfigure the structure of nucleosomes. Until recently, little was known about the structure of these enzymes. Recent progress has revealed that their interaction with chromatin is dominated by ATPase domains that contact DNA at favoured locations on the nucleosome surface. Contacts with histones are limited but play important roles in modulating activity. The ATPase domains do not act in isolation but are flanked by diverse accessory domains and subunits. New structures indicate how these subunits are arranged in multi-subunit complexes providing a framework from which to understand how a common motor is applied to distinct functions.
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8

Strzyz, Paulina. "R loops regulate chromatin remodelling." Nature Reviews Molecular Cell Biology 16, no. 12 (November 18, 2015): 703. http://dx.doi.org/10.1038/nrm4094.

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9

Allison, Susan J. "Chromatin remodelling in diabetic nephropathy." Nature Reviews Nephrology 12, no. 8 (July 18, 2016): 444. http://dx.doi.org/10.1038/nrneph.2016.106.

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10

Flintoft, Louisa. "Chromatin remodelling finds its niche." Nature Reviews Genetics 7, no. 1 (January 2006): 5. http://dx.doi.org/10.1038/nrg1784.

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11

Lafon-Hughes, Laura, María Vittoria Di Tomaso, Leticia Méndez-Acuña, and Wilner Martínez-López. "Chromatin-remodelling mechanisms in cancer." Mutation Research/Reviews in Mutation Research 658, no. 3 (March 2008): 191–214. http://dx.doi.org/10.1016/j.mrrev.2008.01.008.

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12

Farrants, Ann-Kristin Östlund. "Chromatin remodelling and actin organisation." FEBS Letters 582, no. 14 (April 28, 2008): 2041–50. http://dx.doi.org/10.1016/j.febslet.2008.04.032.

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13

Martínez-López, W., and M. V. Di Tomaso. "Chromatin remodelling and chromosome damage distribution." Human & Experimental Toxicology 25, no. 9 (September 2006): 539–45. http://dx.doi.org/10.1191/0960327106het650oa.

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Histone acetylation/deacetylation constitute the most relevant chromatin remodelling mechanism to control DNA access to nuclear machinery as well as to mutagenic agents. Thus, these epigenetics mechanisms could be involved in processing DNA lesions into chromosomal aberrations. Although radiation-induced DNA lesions are believed to occur randomly, in most cases chromosome breakpoints appear distributed in a non-random manner. In order to study the distribution of chromosome damage induced by clastogenic agents in relation to chromosome histone acetylation patterns, an experimental model based on treating Chinese hamster cells with endonucleases and ionizing radiations as well as immunolabelling metaphase chromosomes with antibodies to acetylated histone H4 was developed. The analysis of intra- and interchromosome breakpoint distribution has been carried out on G-banded chromosomes, and results obtained were correlated with chromosome acetylated histone H4 profiles. A co-localization of intrachromosomal breakpoints induced by AluI, BamHI and DNase I as well as by neutrons and g-rays was observed. Radiation- and endonuclease-induced breakpoints tend to cluster in less condensed chromosome regions (G-light bands) that show the highest levels of acetylated histone H4. The analysis of interchromosomal distribution of radiation-induced lesions showed a concentration of breakpoints in Chinese hamster chromosomes with particular histone acetylation patterns. The fact that chromosome breakpoints occur more frequently in transcriptionally competent chromosome regions suggests that chromatin conformation and nuclear architecture could play a role in the distribution of chromosome lesions.
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14

Whitehouse, I., A. Flaus, K. Havas, and T. Owen-Hughes. "Mechanisms for ATP-dependent chromatin remodelling." Biochemical Society Transactions 28, no. 4 (August 1, 2000): 376. http://dx.doi.org/10.1042/0300-5127:0280376.

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15

Flaus, A., I. Whitehouse, K. M. Havas, and T. A. Owen-Hughes. "Mechanisms for ATP-dependent chromatin remodelling." Biochemical Society Transactions 28, no. 3 (June 1, 2000): A62. http://dx.doi.org/10.1042/bst028a062a.

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16

Lavelle, Christophe, and Ralf Blossey. "Chromatin remodelling: why, when & how?" FEBS Journal 278, no. 19 (September 2, 2011): 3578. http://dx.doi.org/10.1111/j.1742-4658.2011.08279.x.

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17

De Vries, M., L. Ramos, Z. Housein, and P. De Boer. "Chromatin remodelling initiation during human spermiogenesis." Biology Open 1, no. 5 (March 27, 2012): 446–57. http://dx.doi.org/10.1242/bio.2012844.

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18

Borg, Michael, and Frédéric Berger. "Chromatin remodelling during male gametophyte development." Plant Journal 83, no. 1 (May 21, 2015): 177–88. http://dx.doi.org/10.1111/tpj.12856.

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19

Noble, Christian. "Chromatin remodelling: it's a tracking business." Trends in Biochemical Sciences 27, no. 11 (November 2002): 548. http://dx.doi.org/10.1016/s0968-0004(02)02205-3.

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20

Flaus, Andrew, and Tom Owen-Hughes. "Mechanisms for ATP-dependent chromatin remodelling." Current Opinion in Genetics & Development 11, no. 2 (April 2001): 148–54. http://dx.doi.org/10.1016/s0959-437x(00)00172-6.

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21

Robyr, D., and A. P. Wolffe. "Review¶Hormone action and chromatin remodelling." Cellular and Molecular Life Sciences CMLS 54, no. 2 (February 1998): 113–24. http://dx.doi.org/10.1007/s000180050130.

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22

Hessmann, Elisabeth, and Volker Ellenrieder. "Chromatin remodelling controls pancreatic tissue fate." Gut 68, no. 7 (March 19, 2019): 1139–40. http://dx.doi.org/10.1136/gutjnl-2018-317486.

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23

Fisher, Alex J., and Keara A. Franklin. "Chromatin remodelling in plant light signalling." Physiologia Plantarum 142, no. 4 (April 29, 2011): 305–13. http://dx.doi.org/10.1111/j.1399-3054.2011.01476.x.

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24

Toto, Maria, Giulia D’Angelo, and Davide F. V. Corona. "Regulation of ISWI chromatin remodelling activity." Chromosoma 123, no. 1-2 (January 12, 2014): 91–102. http://dx.doi.org/10.1007/s00412-013-0447-4.

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25

Richmond, Timothy J. "Nucleosome recognition and spacing by chromatin remodelling factor ISW1a." Biochemical Society Transactions 40, no. 2 (March 21, 2012): 347–50. http://dx.doi.org/10.1042/bst20110748.

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Nucleosomes are actively positioned along DNA by ATP-dependent, chromatin remodelling factors. A structural model for the ISW1a chromatin remodelling factor from Saccharomyces cerevisiae in complex with a dinucleosome substrate was constructed from the X-ray structures of ISW1a (ΔATPase) with and without DNA bound, two different cryo-EM (cryo-electron microscopy) structures of ISW1a (ΔATPase) bound to a nucleosome, and site-directed photo-cross-linking analyses in solution. The X-ray structure of ISW1a (ΔATPase) with DNA bound suggests that DNA sequence may be involved in nucleosome recognition and thereby specificity of promoter interaction. The model suggests how the highly ordered nucleosome arrays observed by mapping nucleosomes in genes and their promoter regions could be generated by a chromatin remodelling factor.
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26

Hager, G. L., T. M. Fletcher, N. Xiao, C. T. Baumann, W. G. Müller, and J. G. McNally. "Dynamics of gene targeting and chromatin remodelling by nuclear receptors." Biochemical Society Transactions 28, no. 4 (August 1, 2000): 405–10. http://dx.doi.org/10.1042/bst0280405.

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Activation of the murine-mammary-tumour virus (MMTV) promoter by the glucocorticoid receptor (GR) is associated with a chromatin structural transition in the B nucleosome region of the viral long terminal repeat (LTR). We have reconstituted this nucleoprotein transition with chromatin assembled on MMTV LTR DNA with Drosophila embryo extracts, purified GR, and HeLa nuclear extract. Chromatin remodelling in vitro is ATP-dependent and maps to a region identical with that found in vivo. We demonstrate specific, glucocorticoid response element dependent, binding of purified GR to a large, multi-nucleosome MMTV chromatin array and show that GR-dependent chromatin remodelling is a multistep process. In the absence of ATP, GR binds to multiple sites on the chromatin array and inhibits nuclease access to GR recognition sites. On the addition of ATP, GR induces remodelling resulting in a large increase in access of enzymes to their sites within the transition region. These findings are complemented by studies in living cells; using a tandem array of MMTV-Ras reporter elements and a form of GR labelled with the green fluorescent protein, we have observed direct targeting of the receptor to response elements in live mouse cells. Whereas the ligand-activated receptor is associated with the MMTV promoter for observable periods, photobleaching experiments provide direct evidence that the hormone-occupied receptor undergoes rapid exchange between chromatin and the nucleoplasmic compartment. The results both in vitro and in vivo are consistent with a dynamic model ('hit and run') in which GR first binds to chromatin after ligand activation, recruits a remodelling activity and is then lost from the template.
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27

Xella, Barbara, Colin Goding, Eleonora Agricola, Ernesto Di Mauro, and Micaela Caserta. "The ISWI and CHD1 chromatin remodelling activities influenceADH2expression and chromatin organization." Molecular Microbiology 59, no. 5 (January 20, 2006): 1531–41. http://dx.doi.org/10.1111/j.1365-2958.2005.05031.x.

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28

Más, Paloma. "Chromatin remodelling and the Arabidopsis biological clock." Plant Signaling & Behavior 3, no. 2 (February 2008): 121–23. http://dx.doi.org/10.4161/psb.3.2.5020.

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29

Whitehouse, Iestyn, Oliver J. Rando, Jeff Delrow, and Toshio Tsukiyama. "Chromatin remodelling at promoters suppresses antisense transcription." Nature 450, no. 7172 (December 2007): 1031–35. http://dx.doi.org/10.1038/nature06391.

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30

Wolffe, A. P. "Corepressor complexes and remodelling chromatin for repression." Biochemical Society Transactions 28, no. 3 (June 1, 2000): A63. http://dx.doi.org/10.1042/bst028a063.

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31

Welsh, Sarah J., and Helen Rizos. "Melanocyte reprogramming requires chromatin and transcription remodelling." Pigment Cell & Melanoma Research 29, no. 3 (March 3, 2016): 260–61. http://dx.doi.org/10.1111/pcmr.12457.

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32

Guyomarc'h, Soazig, Claire Bertrand, Marianne Delarue, and Dao-Xiu Zhou. "Regulation of meristem activity by chromatin remodelling." Trends in Plant Science 10, no. 7 (July 2005): 332–38. http://dx.doi.org/10.1016/j.tplants.2005.05.003.

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33

Gentry, Matthew, and Lars Hennig. "Remodelling chromatin to shape development of plants." Experimental Cell Research 321, no. 1 (February 2014): 40–46. http://dx.doi.org/10.1016/j.yexcr.2013.11.010.

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34

Kollárovič, Gabriel, Caitríona E. Topping, Edward P. Shaw, and Anna L. Chambers. "The human HELLS chromatin remodelling protein promotes end resection to facilitate homologous recombination and contributes to DSB repair within heterochromatin." Nucleic Acids Research 48, no. 4 (December 5, 2019): 1872–85. http://dx.doi.org/10.1093/nar/gkz1146.

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Abstract Efficient double-strand break repair in eukaryotes requires manipulation of chromatin structure. ATP-dependent chromatin remodelling enzymes facilitate different DNA repair pathways, during different stages of the cell cycle and in varied chromatin environments. The contribution of remodelling factors to double-strand break repair within heterochromatin during G2 is unclear. The human HELLS protein is a Snf2-like chromatin remodeller family member and is mutated or misregulated in several cancers and some cases of ICF syndrome. HELLS has been implicated in the DNA damage response, but its mechanistic function in repair is not well understood. We discover that HELLS facilitates homologous recombination at two-ended breaks and contributes to repair within heterochromatic regions during G2. HELLS promotes initiation of HR by facilitating end-resection and accumulation of CtIP at IR-induced foci. We identify an interaction between HELLS and CtIP and establish that the ATPase domain of HELLS is required to promote DSB repair. This function of HELLS in maintenance of genome stability is likely to contribute to its role in cancer biology and demonstrates that different chromatin remodelling activities are required for efficient repair in specific genomic contexts.
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35

Renard, Jean-Paul. "Chromatin remodelling and nuclear reprogramming at the onset of embryonic development in mammals." Reproduction, Fertility and Development 10, no. 8 (1998): 573. http://dx.doi.org/10.1071/rd98086.

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Two main strategies are used to produce cloned mammals. The first involves the condensation of donor chromatin into chromosomes directly exposed to the recipient cytoplasm, whereas the second leaves the donor nucleus in interphase until the time of the first mitosis. Both strategies, which induce marked changes in chromatin organization, allow full reprogrammation of somatic-differentiated fetal and adult cells. This paper reviews some of the recent data that contribute to our understanding of chromatin remodelling at the onset of normal development, as well as after the introduction of a foreign nucleus into a recipient enucleated oocyte. These data indicate that the coordinated changes in chromatin organization that take place up until the first cellular differentiations at the blastocyst stage are determinants for successful cloning. Although some degree of synchronization between the cell cycle stages of donor and recipient cells is necessary for correct remodelling of a transferred nucleus, the kinetics of remodelling events occurring during the one-cell stage appears to be the determining factor for the normal onset of gene expression.
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36

Korber, Philipp, and Peter B. Becker. "Nucleosome dynamics and epigenetic stability." Essays in Biochemistry 48 (September 20, 2010): 63–74. http://dx.doi.org/10.1042/bse0480063.

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Nucleosome remodelling is an essential principle to assure that the packaging of eukaryotic genomes in chromatin remains flexible and adaptable to regulatory needs. Nucleosome remodelling enzymes spend the energy of ATP to alter histone–DNA interactions, to catalyse nucleosome displacement and reassembly, on histone exchange and on the relocation of histone octamers on DNA. Despite these dynamics, chromatin structures encode ‘epigenetic’ information that governs the expression of the underlying genes. These information-bearing structures must be maintained over extended periods of time in resting cells and may be sufficiently stable to resist the turmoil of the cell cycle to be passed on to the next cell generation. Intuitively, nucleosome remodelling should antagonize the maintenance of stable structures. However, upon closer inspection it becomes evident that nucleosome remodelling is intimately involved in the assembly of stable chromatin structures that correspond to functional states. Remodellers may even contribute structural information themselves. Their involvement can be seen at several structural levels: at the levels of positioning individual nucleosomes, homoeostasis of linker histones, histone variants and non-histone proteins, as well as the differential folding of the nucleosome fibre. All of them may contribute to the assembly of heritable epigenetic structures.
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37

Sun, F., F. Tang, A. Y. Yan, H. Y. Fang, and H. Z. Sheng. "Expression of SRG3, a chromatin-remodelling factor, in the mouse oocyte and early preimplantation embryos." Zygote 15, no. 2 (May 2007): 129–38. http://dx.doi.org/10.1017/s096719940600400x.

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SummarySRG3 (Smarcc1) is a core subunit of the SWI/SNF complex. In the absence of SRG3, embryonic development ceases during peri-implantation stages, indicating that SRG3, as well as the chromatin-remodelling process, plays an essential role in early mouse development. To gain a better understanding of chromatin remodelling during the early stages of development, we examined SRG3 expression during oogenesis and preimplantation stages using immunofluorescence and western blot assays. SRG3 was detected in nuclei of oocytes during growth and maturation. Following fertilization, SRG3 was detected in pronuclei shortly after their formation. Nuclear concentrations of SRG3 increased in a time-dependent fashion and were found to be greater in the male pronucleus than in the female pronucleus. The increase in nuclear SRG3 was partially inhibited by a protein synthesis inhibitor, but not by a transcriptional inhibitor. Expression of SRG3 is accompanied by expression of Brg1 and Ini1, two other core subunits of the SWI/SNF complex. The expression of these three remodelling factors parallels that of SP1 and TBP, both spatially and temporally, in the mouse embryo, suggesting a role for remodelling factors in chromatin structure and function during early development.
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38

Pivot-Pajot, Christophe, Cécile Caron, Jérôme Govin, Alexandre Vion, Sophie Rousseaux, and Saadi Khochbin. "Acetylation-Dependent Chromatin Reorganization by BRDT, a Testis-Specific Bromodomain-Containing Protein." Molecular and Cellular Biology 23, no. 15 (August 1, 2003): 5354–65. http://dx.doi.org/10.1128/mcb.23.15.5354-5365.2003.

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ABSTRACT The association between histone acetylation and replacement observed during spermatogenesis prompted us to consider the testis as a source for potential factors capable of remodelling acetylated chromatin. A systematic search of data banks for open reading frames encoding testis-specific bromodomain-containing proteins focused our attention on BRDT, a testis-specific protein of unknown function containing two bromodomains. BRDT specifically binds hyperacetylated histone H4 tail depending on the integrity of both bromodomains. Moreover, in somatic cells, the ectopic expression of BRDT triggered a dramatic reorganization of the chromatin only after induction of histone hyperacetylation by trichostatin A (TSA). We then defined critical domains of BRDT involved in its activity. Both bromodomains of BRDT, as well as flanking regions, were found indispensable for its histone acetylation-dependent remodelling activity. Interestingly, we also observed that recombinant BRDT was capable of inducing reorganization of the chromatin of isolated nuclei in vitro only when the nuclei were from TSA-treated cells. This assay also allowed us to show that the action of BRDT was ATP independent, suggesting a structural role for the protein in the remodelling of acetylated chromatin. This is the first demonstration of a large-scale reorganization of acetylated chromatin induced by a specific factor.
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39

Chiu, Li-Ya, Fade Gong, and Kyle M. Miller. "Bromodomain proteins: repairing DNA damage within chromatin." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1731 (August 28, 2017): 20160286. http://dx.doi.org/10.1098/rstb.2016.0286.

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Genome surveillance and repair, termed the DNA damage response (DDR), functions within chromatin. Chromatin-based DDR mechanisms sustain genome and epigenome integrity, defects that can disrupt cellular homeostasis and contribute to human diseases. An important chromatin DDR pathway is acetylation signalling which is controlled by histone acetyltransferase (HAT) and histone deacetylase (HDAC) enzymes, which regulate acetylated lysines within proteins. Acetylated proteins, including histones, can modulate chromatin structure and provide molecular signals that are bound by acetyl-lysine binders, including bromodomain (BRD) proteins. Acetylation signalling regulates several DDR pathways, as exemplified by the preponderance of HATs, HDACs and BRD proteins that localize at DNA breaks to modify chromatin for lesion repair. Here, we explore the involvement of acetylation signalling in the DDR, focusing on the involvement of BRD proteins in promoting chromatin remodelling to repair DNA double-strand breaks. BRD proteins have widespread DDR functions including chromatin remodelling, chromatin modification and transcriptional regulation. We discuss mechanistically how BRD proteins read acetylation signals within chromatin to trigger DDR and chromatin activities to facilitate genome–epigenome maintenance. Thus, DDR pathways involving BRD proteins represent key participants in pathways that preserve genome–epigenome integrity to safeguard normal genome and cellular functions. This article is part of the themed issue ‘Chromatin modifiers and remodellers in DNA repair and signalling’.
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40

Rashid, Fatema Zahra M., Kathy R. Chaurasiya, Daan J. W. Brocken, and Remus T. Dame. "Regulation of Provwx Transcription By Local Chromatin Remodelling." Biophysical Journal 120, no. 3 (February 2021): 317a. http://dx.doi.org/10.1016/j.bpj.2020.11.2008.

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41

Brewer, Alison C. "Physiological interrelationships between NADPH oxidases and chromatin remodelling." Free Radical Biology and Medicine 170 (July 2021): 109–15. http://dx.doi.org/10.1016/j.freeradbiomed.2021.01.052.

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42

McLay, D. "Remodelling the paternal chromatin at fertilization in mammals." Reproduction 125, no. 5 (May 1, 2003): 625–33. http://dx.doi.org/10.1530/reprod/125.5.625.

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43

Farnung, Lucas, Seychelle M. Vos, Christoph Wigge, and Patrick Cramer. "Nucleosome–Chd1 structure and implications for chromatin remodelling." Nature 550, no. 7677 (October 2017): 539–42. http://dx.doi.org/10.1038/nature24046.

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44

Wolffe, A. P., F. D. Urnov, and D. Guschin. "Co-repressor complexes and remodelling chromatin for repression." Biochemical Society Transactions 28, no. 4 (August 1, 2000): 379. http://dx.doi.org/10.1042/0300-5127:0280379.

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45

Bruns, Alexander-F., Nora Rippaus, Alastair Droop, Muna Al-Jabri, Matthew Care, Michael Jenkinson, Andrew Brodbelt, et al. "Chromatin remodelling to facilitate treatment resistance in glioblastoma." Neuro-Oncology 21, Supplement_4 (October 2019): iv7. http://dx.doi.org/10.1093/neuonc/noz167.027.

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Abstract Recent findings from our group, and the wider community, show that standard treatment does not impose an apparent bottleneck on the clonal evolution of adult glioblastoma (GBM), implying a lack of direct therapeutic opportunity. This does not negate the possibility that multiple treatment-resistance mechanisms co-exist in tumours, repeated across patients, making a combination of targeted therapies a potentially effective approach. We investigated whether treatment resistance may be driven by selection of cellular properties conferred above the level of the genome. Differential expression analysis was performed on 23 pairs of primary and recurrent tumours from patients who received standard treatment and had a local recurrence treated by surgery and second line chemotherapy. This revealed a treatment-induced shift in cell states linked to normal neurodevelopment. The latter is orchestrated by cascades of transcription factors. We, therefore, applied a bespoke gene set enrichment analysis to our paired expression data to investigate whether any factors were implicated in co-regulation of the genes that were altered through therapy. This identified a specific chromatin remodelling machinery, instrumental in normal neurogenesis. We validated our results in an independent cohort of 22 paired GBM samples. Our results suggest that the chromatin remodelling machinery is responsible for determining transcriptional hierarchies in GBM, shown elsewhere to have different treatment sensitivities such that their relative abundances are altered through treatment.
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46

Wolffe, A. P., F. D. Urnov, and D. Guschin. "Co-repressor complexes and remodelling chromatin for repression." Biochemical Society Transactions 28, no. 4 (August 1, 2000): 379–86. http://dx.doi.org/10.1042/bst0280379.

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Recent progress identifies targeted chromatin remodelling by co-repressor complexes as being an integral component of transcriptional silencing. Here we discuss how chromatin structure and the basal transcriptional machinery are manipulated by the co-repressor complex containing the Mi-2 nucleosomal ATPase, the histone-binding protein RbAp48 and histone deacetylase and by the co-repressor complex containing SIN3, RbAp48 and histone deacetylase. Remarkably, both of these complexes also contain methyl-CpG-binding proteins. This observation provides a molecular mechanism to integrate DNA methylation fully into gene control in vertebrates.
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47

Kimmins, Sarah, and Paolo Sassone-Corsi. "Chromatin remodelling and epigenetic features of germ cells." Nature 434, no. 7033 (March 2005): 583–89. http://dx.doi.org/10.1038/nature03368.

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48

Martienssen, Rob, and Steve Henikoff. "The House & Garden guide to chromatin remodelling." Nature Genetics 22, no. 1 (May 1999): 6–7. http://dx.doi.org/10.1038/8708.

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49

Masri, S., R. Orozco-Solis, L. Aguilar-Arnal, M. Cervantes, and P. Sassone-Corsi. "Coupling circadian rhythms of metabolism and chromatin remodelling." Diabetes, Obesity and Metabolism 17 (September 2015): 17–22. http://dx.doi.org/10.1111/dom.12509.

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50

Gregory, Philip D., and Wolfram Hörz. "Life with nucleosomes: chromatin remodelling in gene regulation." Current Opinion in Cell Biology 10, no. 3 (June 1998): 339–45. http://dx.doi.org/10.1016/s0955-0674(98)80009-4.

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