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    Mechanistic modelling supports entwined rather than exclusively competitive DNA double-strand break repair pathway

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    Authors
    Ingram, S
    Warmenhoven, J
    Henthorn, Nicholas
    Smith, E
    Chadwick, A
    Burnet, Neil G
    Mackay, Ranald I
    Kirkby, Norman
    Kirkby, Karen J
    Merchant, Michael J
    Affiliation
    Division of Cancer Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.
    Issue Date
    2019
    
    Metadata
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    Abstract
    Following radiation induced DNA damage, several repair pathways are activated to help preserve genome integrity. Double Strand Breaks (DSBs), which are highly toxic, have specified repair pathways to address them. The main repair pathways used to resolve DSBs are Non-Homologous End Joining (NHEJ) and Homologous Recombination (HR). Cell cycle phase determines the availability of HR, but the repair choice between pathways in the G2 phases where both HR and NHEJ can operate is not clearly understood. This study compares several in silico models of repair choice to experimental data published in the literature, each model representing a different possible scenario describing how repair choice takes place. Competitive only scenarios, where initial protein recruitment determines repair choice, are unable to fit the literature data. In contrast, the scenario which uses a more entwined relationship between NHEJ and HR, incorporating protein co-localisation and RNF138-dependent removal of the Ku/DNA-PK complex, is better able to predict levels of repair similar to the experimental data. Furthermore, this study concludes that co-localisation of the Mre11-Rad50-Nbs1 (MRN) complexes, with initial NHEJ proteins must be modeled to accurately depict repair choice.
    Citation
    Ingram SP, Warmenhoven JW, Henthorn NT, Smith EAK, Chadwick AL, Burnet NG, et al. Mechanistic modelling supports entwined rather than exclusively competitive DNA double-strand break repair pathway. Sci Rep. 2019; 9(1):6359.
    Journal
    Scientific Reports
    URI
    http://hdl.handle.net/10541/621820
    DOI
    10.1038/s41598-019-42901-8
    PubMed ID
    31015540
    Additional Links
    https://dx.doi.org/10.1038/s41598-019-42901-8
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.1038/s41598-019-42901-8
    Scopus Count
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