ArticlePloS one2014
ATM alters the otherwise robust chromatin mobility at sites of DNA double-strand breaks (DSBs) in human cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Crosstalk between chromatin state and ATM signalling in DNA damage-induced transcription stress.The EMBO journal · 2025Article
- Disparate Pathways for Extrachromosomal DNA Biogenesis and Genomic DNA Repair.Cancer discovery · 2025Article
- Disparate pathways for extrachromosomal DNA biogenesis and genomic DNA repair.bioRxiv : the preprint server for biology · 2023Article
- The plant-specific DDR factor SOG1 increases chromatin mobility in response to DNA damage.EMBO reports · 2022Article
- To indel or not to indel: Factors influencing mutagenesis during chromosomal break end joining.DNA repair · 2022Review
- Review
- Collaborations between chromatin and nuclear architecture to optimize DNA repair fidelity.DNA repair · 2021Review
- Monitoring global changes in chromatin compaction states upon localized DNA damage with tools of fluorescence anisotropy.Molecular biology of the cell · 2020Article
- Structural and Dynamical Signatures of Local DNA Damage in Live Cells.Biophysical journal · 2020Article
- Article
- Complex Chromatin Motions for DNA Repair.Frontiers in genetics · 2020Review
- Review
- Keep moving and stay in a good shape to find your homologous recombination partner.Current genetics · 2019Review
- Quantifying site-specific chromatin mechanics and DNA damage response.Scientific reports · 2018Article
- Cis- and Trans-Modifiers of Repeat Expansions: Blending Model Systems with Human Genetics.Trends in genetics : TIG · 2018Review
- Live Dynamics of 53BP1 Foci Following Simultaneous Induction of Clustered and Dispersed DNA Damage in U2OS Cells.International journal of molecular sciences · 2018Article
- And yet, it moves: nuclear and chromatin dynamics of a heterochromatic double-strand break.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Chromatin Dynamics in Genome Stability: Roles in Suppressing Endogenous DNA Damage and Facilitating DNA Repair.International journal of molecular sciences · 2017Review
- Genome-wide mapping of long-range contacts unveils clustering of DNA double-strand breaks at damaged active genes.Nature structural & molecular biology · 2017Article
- Regulation of pairing between broken DNA-containing chromatin regions by Ku80, DNA-PKcs, ATM, and 53BP1.Scientific reports · 2017Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ionizing radiation induces DNA double strand breaks (DSBs) which can lead to the formation of chromosome rearrangements through error prone repair. In mammalian cells the positional stability of chromatin contributes to the maintenance of genome integrity. DSBs exhibit only a small, submicron scale diffusive mobility, but a slight increase in the mobility of chromatin domains by the induction of DSBs might influence repair fidelity and the formation of translocations. The radiation-induced local DNA decondensation in the vicinity of DSBs is one factor potentially enhancing the mobility of DSB-containing chromatin domains. Therefore in this study we focus on the influence of different chromatin modifying proteins, known to be activated by the DNA damage response, on the mobility of DSBs. IRIF (ionizing radiation induced foci) in U2OS cells stably expressing 53BP1-GFP were used as a surrogate marker of DSBs. Low angle charged particle irradiation, known to trigger a pronounced DNA decondensation, was used for the defined induction of linear tracks of IRIF. Our results show that movement of IRIF is independent of the investigated chromatin modifying proteins like ACF1 or PARP1 and PARG. Also depletion of proteins that tether DNA strands like MRE11 and cohesin did not alter IRIF dynamics significantly. Inhibition of ATM, a key component of DNA damage response signaling, resulted in a pronounced confinement of DSB mobility, which might be attributed to a diminished radiation induced decondensation. This confinement following ATM inhibition was confirmed using X-rays, proving that this effect is not restricted to densely ionizing radiation. In conclusion, repair sites of DSBs exhibit a limited mobility on a small spatial scale that is mainly unaffected by depletion of single remodeling or DNA tethering proteins. However, it relies on functional ATM kinase which is considered to influence the chromatin structure after irradiation.
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