hCAS/CSE1L regulates RAD51 distribution and focus formation for homologous recombinational repair

Satoshi Okimoto, Jiying Sun, Atsuhiko Fukuto, Yasunori Horikoshi, Shun Matsuda, Tomonari Matsuda, Masae Ikura, Tsuyoshi Ikura, Shinichi Machida, Hitoshi Kurumizaka, Yoichi Miyamoto, Masahiro Oka, Yoshihiro Yoneda, Yoshiaki Kiuchi, Satoshi Tashiro

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    5 Citations (Scopus)

    Abstract

    Homologous recombinational repair (HR) is one of the major repair systems for DNA double-strand breaks. RAD51 is a key molecule in HR, and the RAD51 concentration in the cell nucleus increases after DNA damage induction. However, the mechanism that regulates the intracellular distribution of RAD51 is still unclear. Here, we show that hCAS/CSE1L associates with RAD51 in human cells. We found that hCAS/CSE1L negatively regulates the nuclear protein level of RAD51 under normal conditions. hCAS/CSE1L is also required to repress the DNA damage-induced focus formation of RAD51. Moreover, we show that hCAS/CSE1L plays roles in the regulation of the HR activity and in chromosome stability. These findings suggest that hCAS/CSE1L is responsible for controlling the HR activity by directly interacting with RAD51. We found that hCAS/CSE1L regulates the nuclear concentration of RAD51 and nuclear RAD51 focus formation. hCAS/CSE1L was required to repress the HR activity and to keep chromosome stability. These findings suggest that hCAS/CSE1L is responsible for genome integrity by regulating the intracellular distribution of RAD51.

    Original languageEnglish
    Pages (from-to)681-694
    Number of pages14
    JournalGenes to Cells
    Volume20
    Issue number9
    DOIs
    Publication statusPublished - 2015 Sep 1

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    ASJC Scopus subject areas

    • Genetics
    • Cell Biology

    Cite this

    Okimoto, S., Sun, J., Fukuto, A., Horikoshi, Y., Matsuda, S., Matsuda, T., Ikura, M., Ikura, T., Machida, S., Kurumizaka, H., Miyamoto, Y., Oka, M., Yoneda, Y., Kiuchi, Y., & Tashiro, S. (2015). hCAS/CSE1L regulates RAD51 distribution and focus formation for homologous recombinational repair. Genes to Cells, 20(9), 681-694. https://doi.org/10.1111/gtc.12262