Earlier work from the laboratory of Susan Gasser had noted changes in the physical behavior of chromatin when it incurred DNA damage: loci bearing double-strand breaks showed enhanced movement, becoming highly dynamic. Furthermore, the same effect could be observed with undamaged sites in a cell nucleus responding to DNA damage. Getting to the root cause of this phenomenon, Michael Hauer, a PhD student in her group discovered that histones dissociate from DNA and roughly 30% of the entire complement are degraded upon DNA damage. The process is controlled by the so-called checkpoint response, and the reduction in nucleosome density not only increases DNA mobility but also leads to increased chromatin accessibility for recombination-mediated repair.