**Author details**

**3.5. Modifications of chromatin compaction in response to DSB and perspectives**

the precise role of each step remains to be elucidated.

tions in the direction of the tangent are lost.

DNA damage.

58 Chromatin and Epigenetics

**4. Conclusion**

length.

In addition to chromatin mobility, many studies investigated the modulation of the chromatin compaction state both at a specific damaged site and throughout the genome. Several studies showed a chromatin decondensation visible at the micrometer scale accessible by conventional light microscopy [85, 99]. In the recent studies, super resolution imaging of a *lacO* array before and after damage allows the visualization of chromatin decompaction at the damaged site in haploid yeast [90, 100]. In mammalian cells, most of the studies report chromatin decondensation at the damaged site. However, it has been shown that following this initial fast decondensation, the damaged chromatin area slowly recondenses to reach higher compaction levels than before damage induction [101]. In addition, both chromatin expansion and compaction occur at the same time but in different regions of the chromatin near the DSBs [49]. Overall, chromatin changes in compaction are tuned in space and time upon DSBs, but

An interesting way to interpret chromatin changes in dynamics and compaction upon DSBs is to think in terms of mechanical properties of chromatin, such as chromatin stiffness (or persistence length). As illustrated in **Figure 4**, the persistence length of a polymer is a mechanical property that quantifies its stiffness. The persistence length is the length over which correla-

Changes in chromatin persistence length following DNA damage have been discussed, however, with contradictories interpretations. While some studies suggest that chromatin is more flexible following DSBs [100, 102, 103], other results indicate that chromatin is globally stiffer upon DSBs [65, 90]. One proposed explanation for chromatin stiffening upon DSBs could be the presence of negative charges due to H2A S129 phosphorylation [90]. Further studies will be required to solve to this open question and more generally to understand the physical mechanisms underlying the modifications of chromatin dynamics in response to

Thanks to recent advanced in fast and high-resolution microscopy, it became possible to quantify chromatin mobility with unprecedented precision and to understand how chromatin

**Figure 4.** Illustration of the persistence of a polymer, where Lp is the polymer persistence length and L is the polymer

Judith Miné-Hattab1,2\* and Xavier Darzacq3

\*Address all correspondence to: judith.mine@curie.fr

1 Institut Curie, PSL Research University, CNRS, UMR3664, Paris, France

2 Institut Curie, Sorbonne Université, CNRS, UMR3664, Paris, France

3 Department of Molecular and Cell Biology, Li Ka Shing Center for Biomedical and Health Sciences, CIRM Center of Excellence, University of California, Berkeley, United States
