NDLI: Spatiotemporal characterization of ionizing radiation induced DNA damage foci and their relation to chromatin organization.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Costes, S. V. Chiolo, I. Pluth, J. M. Barcellos-Hoff, M. H. Jakob, B.
Description	Country affiliation: United States Author Affiliation: Costes SV ( Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA. svcostes@lbl.gov)
Abstract	DNA damage sensing proteins have been shown to localize to the sites of DNA double strand breaks (DSB) within seconds to minutes following ionizing radiation (IR) exposure, resulting in the formation of microscopically visible nuclear domains referred to as radiation-induced foci (RIF). This review characterizes the spatiotemporal properties of RIF at physiological doses, minutes to hours following exposure to ionizing radiation, and it proposes a model describing RIF formation and resolution as a function of radiation quality and chromatin territories. Discussion is limited to RIF formed by three interrelated proteins ATM (Ataxia telangiectasia mutated), 53BP1 (p53 binding protein 1) and gammaH2AX (phosphorylated variant histone H2AX), with an emphasis on the later. This review discusses the importance of not equating RIF with DSB in all situations and shows how dose and time dependence of RIF frequency is inconsistent with a one to one equivalence. Instead, we propose that RIF mark regions of the chromatin that would serve as scaffolds rigid enough to keep broken DNA from diffusing away, but open enough to allow the repair machinery to access the damage site. We review data indicating clear kinetic and physical differences between RIF emerging from dense and uncondensed regions of the nucleus. We suggest that persistent RIF observed days following exposure to ionizing radiation are nuclear marks of permanent rearrangement of the chromatin architecture. Such chromatin alterations may not always lead to growth arrest as cells have been shown to replicate these in progeny. Thus, heritable persistent RIF spanning over tens of Mbp may reflect persistent changes in the transcriptome of a large progeny of cells. Such model opens the door to a 'non-DNA-centric view' of radiation-induced phenotypes.
File Format	HTM / HTML
ISSN	13835718
e-ISSN	18793592
DOI	10.1016/j.mrrev.2009.12.006
Journal	Mutation Research/Genetic Toxicology and Environmental Mutagenesis
Issue Number	1-3
Volume Number	704
Language	English
Publisher	Elsevier
Publisher Date	2010-04-01
Publisher Place	Netherlands
Access Restriction	Open
Subject Keyword	Models, Theoretical Research Support, U.s. Gov't, Non-p.h.s. Chromatin Dna Repair Discipline Genetics Dna-binding Proteins Intracellular Signaling Peptides And Proteins Dose-response Relationship, Radiation Dna Breaks, Double-stranded Discipline Biochemistry Protein-serine-threonine Kinases Ataxia Telangiectasia Mutated Proteins Metabolism Dna Damage Ultrastructure Chromatin Assembly And Disassembly Histones Cell Cycle Proteins Tumor Suppressor Proteins
Content Type	Text
Resource Type	Article
Subject	Genetics Health, Toxicology and Mutagenesis

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DNA damage signaling in response to double-strand breaks during mitosis

Inter-individual variation in DNA double-strand break repair in human fibroblasts before and after exposure to low doses of ionizing radiation.

Regulation of ATM in DNA double strand break repair accounts for the radiosensitivity in human cells exposed to high linear energy transfer ionizing radiation.

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Telomere shortening alters the kinetics of the DNA damage response after ionizing radiation in human cells

PTIP regulates 53BP1 and SMC1 at the DNA damage sites.

Drosophila ATM and ATR have distinct activities in the regulation of meiotic DNA damage and repair

Heme oxygenase-1 and carbon monoxide modulate DNA repair through ataxia-telangiectasia mutated (ATM) protein.

Autophosphorylation at serine 1981 stabilizes ATM at DNA damage sites

Spatiotemporal characterization of ionizing radiation induced DNA damage foci and their relation to chromatin organization.

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