Essential role of Tip60-dependent recruitment of ribonucleotide reductase at DNA damage sites in DNA repair during G1 phase

DOI
  • NIIDA Hiroyuki
    Department of Cell Biology, Graduate School of Medical Sciences, Nagoya City University Medical School Department of Biochemistry 1, Hamamatsu University School of Medicine
  • KATSUNO Yuko
    Department of Cell Biology, Graduate School of Medical Sciences, Nagoya City University Medical School
  • SENGOKU Misuzu
    Department of Cell Biology, Graduate School of Medical Sciences, Nagoya City University Medical School
  • YUKAWA Megumi
    Department of Cell Biology, Graduate School of Medical Sciences, Nagoya City University Medical School
  • SHIMADA Midori
    Department of Cell Biology, Graduate School of Medical Sciences, Nagoya City University Medical School
  • IKURA Masae
    Radiatrion Biology Center, Kyoto University
  • IKURA Tsuyoshi
    Radiatrion Biology Center, Kyoto University
  • KOHNO Kazuteru
    Department of Cell Biology, RIRBM, Hiroshima University
  • SHIMA Hiroki
    Department of Cell Biology, RIRBM, Hiroshima University
  • SUZUKI Hidekazu
    Department of Cell Biology, RIRBM, Hiroshima University
  • TASHIRO Satoshi
    Department of Cell Biology, RIRBM, Hiroshima University
  • KITAGAWA Masatoshi
    Department of Biochemistry 1, Hamamatsu University School of Medicine
  • NAKANISHI Makoto
    Department of Cell Biology, Graduate School of Medical Sciences, Nagoya City University Medical School

Bibliographic Information

Other Title
  • G１期DNA修復においてダメージ部位へのTip60依存的ribonucleotide reductase集積は必須である

Abstract

A balanced deoxyribonucleotides (dNTPs) supply is essential for DNA repair. Here, we found that ribonucleotide reductase (RNR) subunits, RRM1 and RRM2, accumulated very rapidly at damage sites. RRM1 physically bound to Tip60. ChIP analyses of cells with an I-SceI cassette revealed that RRM1 bound to a damage site in a Tip60-dependent manner. Active RRM1 mutants lacking Tip60 binding failed to rescue an impaired DNA repair in RRM1-depleted G1 phase cells. Inhibition of RNR recruitment by RRM1 C-terminal fragment sensitized cells to DNA damage. We propose that Tip60-dependent recruitment of RNR plays an essential role in dNTPs supply for DNA repair.

Journal

Keywords

Details 詳細情報について

  • CRID
    1390282680616961024
  • NII Article ID
    130007000033
  • DOI
    10.11513/jrrsabst.2010.0.64.0
  • Text Lang
    ja
  • Data Source
    • JaLC
    • CiNii Articles
  • Abstract License Flag
    Disallowed

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