Fig. 6.

A model for DSB repair status under low ATP condition. ATP is involved in several steps in DSB repair, such as DNA ligation, chromatin remodeling and DNA damage signaling via protein kinase and ATPase activities. In addition, DNA nucleases and DNA helicases, which are critical enzymes promoting DSB repair, require ATP. This study showed that short-term ATP shortage reduces DSB end resection and almost completely impaired RAD51 recruitment in G2 cells after IR. The impairment of RAD51 loading may be dependent on the lack of multiple pathways in HR process such as DNA nuclease- and DNA helicase-dependent DSB end processing and chromatin remodeling.