Cell lines derived from a Medaka radiation-sensitive mutant have defects in DNA double-strand break responses

Masayuki Hidaka, Shoji Oda, Yoshikazu Kuwahara, Manabu Fukumoto, Hiroshi Mitani

研究成果: Article査読

15 被引用数 (Scopus)

抄録

It was reported that the radiation-sensitive Medaka mutant "ric1" has a defect in the repair of DNA double-strand breaks (DSBs) induced by γ-rays during early embryogenesis. To study the cellular response of a ric1 mutant to ionizing radiation (IR), we established the mutant embryonic cell lines RIC1-e9, RIC1- e42, RIC1-e43. Following exposure to γ-irradiation, the DSBs in wild-type cells were repaired within 1 h, while those in RIC1 cells were not rejoined even after 2 h. Cell death was induced in the wild-type cells with cell fragmentation, but only a small proportion of the RIC1 cells underwent cell death, and without cell fragmentation. Although both wild-type and RIC1 cells showed mitotic inhibition immediately after γ- irradiation, cell division was much slower to resume in the wild-type cells (20 h versus 12 h). In both wild-type and RIC1 cells, Ser139 phosphorylated H2AX (γH2AX) foci were formed after γ-irradiation, however, the γH2AX foci disappeared more quickly in the RIC1 cell lines. These results suggest that the instability of γH2AX foci in RIC1 cells cause an aberration of the DNA damage response. As RIC1 cultured cells showed similar defective DNA repair as ric1 embryos and RIC1 cells revealed defective cell death and cell cycle checkpoint, they are useful for investigating DNA damage responses in vitro.

本文言語English
ページ(範囲)165-171
ページ数7
ジャーナルJournal of radiation research
51
2
DOI
出版ステータスPublished - 2010 3 25

ASJC Scopus subject areas

  • 放射線
  • 放射線学、核医学およびイメージング
  • 健康、毒物学および変異誘発

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