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      ISWI chromatin remodeling complexes in the DNA damage response

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          Abstract

          Regulation of chromatin structure is an essential component of the DNA damage response (DDR), which effectively preserves the integrity of DNA by a network of multiple DNA repair and associated signaling pathways. Within the DDR, chromatin is modified and remodeled to facilitate efficient DNA access, to control the activity of repair proteins and to mediate signaling. The mammalian ISWI family has recently emerged as one of the major ATP-dependent chromatin remodeling complex families that function in the DDR, as it is implicated in at least 3 major DNA repair pathways: homologous recombination, non-homologous end-joining and nucleotide excision repair. In this review, we discuss the various manners through which different ISWI complexes regulate DNA repair and how they are targeted to chromatin containing damaged DNA.

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          Most cited references 83

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          The biology of chromatin remodeling complexes.

          The packaging of chromosomal DNA by nucleosomes condenses and organizes the genome, but occludes many regulatory DNA elements. However, this constraint also allows nucleosomes and other chromatin components to actively participate in the regulation of transcription, chromosome segregation, DNA replication, and DNA repair. To enable dynamic access to packaged DNA and to tailor nucleosome composition in chromosomal regions, cells have evolved a set of specialized chromatin remodeling complexes (remodelers). Remodelers use the energy of ATP hydrolysis to move, destabilize, eject, or restructure nucleosomes. Here, we address many aspects of remodeler biology: their targeting, mechanism, regulation, shared and unique properties, and specialization for particular biological processes. We also address roles for remodelers in development, cancer, and human syndromes.
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            Histone H4-K16 acetylation controls chromatin structure and protein interactions.

            Acetylation of histone H4 on lysine 16 (H4-K16Ac) is a prevalent and reversible posttranslational chromatin modification in eukaryotes. To characterize the structural and functional role of this mark, we used a native chemical ligation strategy to generate histone H4 that was homogeneously acetylated at K16. The incorporation of this modified histone into nucleosomal arrays inhibits the formation of compact 30-nanometer-like fibers and impedes the ability of chromatin to form cross-fiber interactions. H4-K16Ac also inhibits the ability of the adenosine triphosphate-utilizing chromatin assembly and remodeling enzyme ACF to mobilize a mononucleosome, indicating that this single histone modification modulates both higher order chromatin structure and functional interactions between a nonhistone protein and the chromatin fiber.
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              Regulation of nucleosome dynamics by histone modifications.

              Chromatin is a dynamic structure that must respond to myriad stimuli to regulate access to DNA, and chemical modification of histones is a major means by which the cell modulates nucleosome mobility and turnover. Histone modifications are linked to essentially every cellular process requiring DNA access, including transcription, replication and repair. Here we consider properties of the major types of histone modification in the context of their associated biological processes to view them in light of the cellular mechanisms that regulate nucleosome dynamics.
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                Author and article information

                Journal
                Cell Cycle
                Cell Cycle
                KCCY
                Cell Cycle
                Taylor & Francis
                1538-4101
                1551-4005
                1 October 2014
                30 October 2014
                : 13
                : 19
                : 3016-3025
                Affiliations
                Department of Genetics; Cancer Genomics Netherlands; Erasmus MC ; Rotterdam, The Netherlands
                Author notes
                [* ]Correspondance to: Hannes Lans; Email: w.lans@ 123456erasmusmc.nl
                Article
                956551
                10.4161/15384101.2014.956551
                4615051
                25486562
                © 2014 The Author(s). Published with license by Taylor & Francis Group, LLC© Özge Z Aydin, Wim Vermeulen, and Hannes Lans

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

                Page count
                Figures: 4, Tables: 0, References: 104, Pages: 10
                Product
                Funding
                This work was supported by the Association for International Cancer Research (grant number 08-0084), the Netherlands Organization for Scientific Research (ALW grant numbers 863.08.022, 854.11.002 and ZonMW 912.12.132) and the European Research Council Advanced Grants (grant number 340988 – ERC_ID to WV).
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