Article: article from journal or magazin.
Checkpoint kinases and the INO80 nucleosome remodeling complex enhance global chromatin mobility in response to DNA damage.
Genes and Development
Double-strand break repair by recombination requires a homology search. In yeast, induced breaks move significantly more than undamaged loci. To examine whether DNA damage provokes an increase in chromatin mobility generally, we tracked undamaged loci under DNA-damaging conditions. We found that the yeast checkpoint factors Mec1, Rad9, and Rad53 are required for genome-wide increases in chromatin mobility, but not the repair protein Rad51. Mec1 activation by targeted Ddc1/Ddc2 enhances chromatin mobility even in the absence of damage. Finally, the INO80 chromatin remodeler is shown to act downstream from Mec1 to increase chromatin mobility, highlighting an additional damage-related role of this nucleosome remodeling complex.
Cell Cycle Checkpoints/physiology, Cell Cycle Proteins/genetics, Cell Cycle Proteins/metabolism, Chromatin/metabolism, DNA Damage, Genome, Fungal/genetics, Models, Biological, Phosphotransferases/metabolism, Saccharomyces cerevisiae/enzymology, Saccharomyces cerevisiae/genetics, Saccharomyces cerevisiae Proteins/genetics, Saccharomyces cerevisiae Proteins/metabolism
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