Rxivist logo

A limited number of double-strand DNA breaks are sufficient to delay cell cycle progression.

By Jeroen van den Berg, Anna G. Manjón, Karoline Kielbassa, Femke M Feringa, Raimundo Freire, René H. Medema

Posted 07 May 2018
bioRxiv DOI: 10.1101/316158 (published DOI: 10.1093/nar/gky786)

DNA damaging agents cause a variety of lesions, of which DNA double-strand breaks (DSBs) are the most genotoxic. Unbiased approaches aimed at investigating the relationship between the number of DSBs and outcome of the DNA damage response have been challenging due to the random nature in which damage is induced by classical DNA damaging agents. Here we describe a CRISPR/Cas9-based system that permits us to efficiently introduce DSBs at defined sites in the genome. Using this system, we show that a guide RNA targeting only a single site in the human genome can trigger a checkpoint response that is potent enough to delay cell cycle progression. Abrogation of this checkpoint leads to DNA breaks in mitosis which give rise to micronucleated daughter cells.

Download data

  • Downloaded 834 times
  • Download rankings, all-time:
    • Site-wide: 15,029 out of 88,403
    • In cell biology: 633 out of 4,523
  • Year to date:
    • Site-wide: 61,385 out of 88,403
  • Since beginning of last month:
    • Site-wide: 77,455 out of 88,403

Altmetric data

Downloads over time

Distribution of downloads per paper, site-wide


Sign up for the Rxivist weekly newsletter! (Click here for more details.)