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Increased mobility of double-strand breaks requires Mec1, Rad9 and the homologous recombination machinery.
Nature Cell Biology
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.
Cell Cycle Proteins/physiology, Chromatin/metabolism, DNA Damage, Intracellular Signaling Peptides and Proteins/physiology, Microscopy, Fluorescence, Protein-Serine-Threonine Kinases/physiology, Recombination, Genetic, Saccharomyces cerevisiae/metabolism, Saccharomyces cerevisiae Proteins/physiology
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