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Increased mobility of double-strand breaks requires Mec1, Rad9 and the homologous recombination machinery

Dion, Vincent, Kalck, Véronique, Horigome, Chihiro, Towbin, Benjamin D. and Gasser, Susan M. 2012. Increased mobility of double-strand breaks requires Mec1, Rad9 and the homologous recombination machinery. Nature Cell Biology 14 (5) , 502--509. 10.1038/ncb2465

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Abstract

Chromatin mobility is thought to facilitate homology search during homologous recombination and to shift damage either towards or away from specialized repair compartments. However, unconstrained mobility of double-strand breaks could also promote deleterious chromosomal translocations. Here we use live time-lapse fluorescence microscopy to track the mobility of damaged DNA in budding yeast. We found that a Rad52–YFP focus formed at an irreparable double-strand break moves in a larger subnuclear volume than the undamaged locus. In contrast, Rad52–YFP bound at damage arising from a protein–DNA adduct shows no increase in movement. Mutant analysis shows that enhanced double-strand-break mobility requires Rad51, the ATPase activity of Rad54, the ATR homologue Mec1 and the DNA-damage-response mediator Rad9. Consistent with a role for movement in the homology-search step of homologous recombination, we show that recombination intermediates take longer to form in cells lacking Rad9.

Item Type: Article
Status: Published
Schools: Medicine
Publisher: Nature Publishing Group
ISSN: 1465-7392
Last Modified: 26 Mar 2019 11:13
URI: http://orca-mwe.cf.ac.uk/id/eprint/120289

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