Shunya Takada

Publications (2)0.95 Total impact

• Article: A novel role for Rad17 in homologous recombination.

  Katsuaki Nishino, Eri Inoue, Shunya Takada, Takuya Abe, Motomu Akita, Akari Yoshimura, Shusuke Tada, Masahiko Kobayashi, Ken-Ichi Yamamoto, Masayuki Seki, Takemi Enomoto
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  ABSTRACT: Replication checkpoint protein Rad17 senses DNA lesions during DNA replication and halts progression of replication fork. The cells derived from Bloom syndrome individuals show some defects in DNA replication. In order to investigate the functional relationship between the replication checkpoint protein Rad17 and BLM, which is the product of the causative gene of Bloom syndrome, we generated BLM/RAD17 double knockout (blm/rad17) cells using chicken DT40 cells. The blm/rad17 cells showed exaggerated growth defects as determined by analysis of their growth curves and plating efficiency compared to those of either of the single gene mutants. These defects seem to be due to an increase in DNA lesions that cause spontaneous cell death, suggesting that Rad17 and BLM execute different functions in the progression of replication forks. We also demonstrate that targeting integration was dramatically compromised by a lack of Rad17. In addition, the elevated frequency of sister chromatid exchange (SCE) due to homologous recombination in BLM knockout (blm) cells was greatly reduced by disruption of the RAD17 gene. Thus, in addition to its role in the replication checkpoint, Rad17 appears to play a role in homologous recombination.
  Genes & Genetic Systems 11/2008; 83(5):427-31. · 0.95 Impact Factor
• Article: Generation and characterization of cells that can be conditionally depleted of mitochondrial SOD2

  Shunya Takada, Eri Inoue, Keizo Tano, Hanako Yoshii, Takuya Abe, Akari Yoshimura, Motomu Akita, Shusuke Tada, Masami Watanabe, Masayuki Seki, Takemi Enomoto
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  ABSTRACT: Manganese-dependent superoxide dismutase (SOD2) serves as the primary defense against mitochondrial superoxide, and decreased SOD2 activity results in a range of pathologies. To investigate the events occurring soon after depletion of SOD2, we generated SOD2 gene knockout chicken DT40 cells complemented with a human SOD2 (hSOD2) cDNA, whose expression can be switched off by doxycycline (Dox). When SOD2 was depleted by the addition of Dox, the cells grew slightly slower and formed fewer colonies than cells expressing hSOD2. In addition, these cells showed a high sensitivity to paraquat, which produces superoxide, and died through apoptosis. In contrast to results obtained with mouse and DrosophilaSod2 mutants, we found no indication of an increase in DNA lesions due to depletion of SOD2.
  Biochemical and Biophysical Research Communications.