Ubiquitin and SUMO DNA damage response signalling at deprotected telomeres during the cell cycle

基因组损伤后，细胞停止分裂并开始DNA修复。我们发现，在细胞分裂的特定时间，如果损伤信号来自染色体末端（即“端粒”），则不会发生这种情况。我们预计这对于防止健康细胞的基因组不稳定是必要的，并且可能会导致癌细胞的基因组不稳定。这里描述的实验将阐明我们观察到的分子机制和生物学意义。

Following genome damage cells stop the cell division process and initiate DNA repair. We discovered that at specific times during cell division his does not happen if the damage signals originate from the chromosome ends (i.e. “telomeres”). We anticipate this is necessary to prevent genomic instability in healthy cells and may be driving genomic instability in cancer cells. Experiments described here will elucidate the molecular mechanisms and biological significance of our observation.