hCAS / CSE 1L regulates RAD 51 distribution and focus formation for homologous recombinational repair

Homologous recombinational repair ( HR ) is one of the major repair systems for DNA double‐strand breaks. RAD 51 is a key molecule in HR , and the RAD 51 concentration in the cell nucleus increases after DNA damage induction. However, the mechanism that regulates the intracellular distribution of RAD 51 is still unclear. Here, we show that hCAS / CSE 1L associates with RAD 51 in human cells. We found that hCAS / CSE 1L negatively regulates the nuclear protein level of RAD 51 under normal conditions. hCAS / CSE 1L is also required to repress the DNA damage‐induced focus formation of RAD 51. Moreover, we show that hCAS / CSE 1L plays roles in the regulation of the HR activity and in chromosome stability. These findings suggest that hCAS / CSE 1L is responsible for controlling the HR activity by directly interacting with RAD 51.