A break in both strands of the DNA double helix is potentially very dangerous for organisms because the free ends can recombine inappropriately with other parts of the genome and cause substantial damage. Eukaryotic cells sense and attempt to repair such breaks very rapidly, through the recruitment of DNA repair proteins to the sites of damage, forming nuclear repair foci. Soutoglou and Misteli have tethered various repair factors individually to unbroken DNA in human tissue culture cells and find that, surprisingly, even in the absence of DNA damage, repair foci form at the tether site. The DNA damage response may thus involve amplification of the damage signaling cascade, and the damage-sensing proteins may detect alterations in the higher-order structure of chromatin around the break.
- Damage Detection
Protein complexes that usually assemble on and repair damaged DNA can form at undamaged sites to halt the cell cycle if several of the proteins are first tethered there.Permalink: