Friedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland;
Genes Dev. 2013 Sep 15;27(18):1999-2008. doi: 10.1101/gad.222992.113. Epub 2013 Sep 12.
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.
双链断裂修复需要通过同源重组进行，该过程需要进行同源搜索。在酵母中，诱导产生的双链断裂比未损伤的基因座移动得更远。为了研究 DNA 损伤是否普遍引起染色质流动性增加，我们在 DNA 损伤条件下检测了未损伤的基因座。我们发现，酵母检查点因子 Mek1、Rad9 和 Rad53 对于全基因组染色质流动性的增加是必需的，但修复蛋白 Rad51 不是必需的。即使没有损伤，靶向 Ddc1/Ddc2 激活 Mek1 也能增强染色质流动性。最后，INO80 染色质重塑因子被证明作用于 Mek1 下游，以增加染色质流动性，这突出了该核小体重塑复合物的另一个与损伤相关的作用。
