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タイトル
  • en The CST complex facilitates cell survival under oxidative genotoxic stress
作成者
アクセス権 open access
権利情報
  • en © 2023 Hara et al.
  • http://creativecommons.org/licenses/by/4.0/
  • en This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
主題
  • Other en DNA damage
  • Other en DNA replication
  • Other en Synthesis phase
  • Other en HeLa cells
  • Other en DNA repair
  • Other en Cell cycle and cell division
  • Other en Cell staining
  • Other en Flow cytometry
内容注記
  • Abstract en Genomic DNA is constantly exposed to a variety of genotoxic stresses, and it is crucial for organisms to be equipped with mechanisms for repairing the damaged genome. Previously, it was demonstrated that the mammalian CST (CTC1-STN1-TEN1) complex, which was originally identified as a single-stranded DNA-binding trimeric protein complex essential for telomere maintenance, is required for survival in response to hydroxyurea (HU), which induces DNA replication fork stalling. It is still unclear, however, how the CST complex is involved in the repair of diverse types of DNA damage induced by oxidizing agents such as H₂O₂. STN1 knockdown (KD) sensitized HeLa cells to high doses of H₂O₂. While H₂O₂ induced DNA strand breaks throughout the cell cycle, STN1 KD cells were as resistant as control cells to H₂O₂ treatment when challenged in the G1 phase of the cell cycle, but they were sensitive when exposed to H₂O₂ in S/G2/M phase. STN1 KD cells showed a failure of DNA synthesis and RAD51 foci formation upon H₂O₂ treatment. Chemical inhibition of RAD51 in shSTN1 cells did not exacerbate the sensitivity to H₂O₂, implying that the CST complex and RAD51 act in the same pathway. Collectively, our results suggest that the CST complex is required for maintaining genomic stability in response to oxidative DNA damage, possibly through RAD51-dependent DNA repair/protection mechanisms.
出版者 en Public Library of Science (PLoS)
日付
    Issued2023-08
言語
  • eng
資源タイプ journal article
出版タイプ VoR
資源識別子 HDL http://hdl.handle.net/2433/286526
関連
  • isIdenticalTo DOI https://doi.org/10.1371/journal.pone.0289304
  • isIdenticalTo PMID 37590191
助成情報
  • 助成機関名 ja 日本学術振興会
  • 研究課題番号 JP19H05655 https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-19H05655/ JGN
  • 研究課題名 ja 微小環境変動に対する細胞応答に着目した治癒をめざした抗腫瘍療法
  • 助成機関名 ja 日本学術振興会
  • 研究課題番号 JP21K19219 https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21K19219/ JGN
  • 研究課題名 ja ノンコーディング配列Aluレトロトランスポゾンの転移制御因子の探索
  • 助成機関名 ja 日本学術振興会
  • 研究課題番号 JP22H02600 https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22H02600/ JGN
  • 研究課題名 ja ゲノム破壊と創生サイクルを生み出すヒトLINE-1の制御機構の解明
収録誌情報
    • EISSN 1932-6203
      • en PLOS ONE
      • 巻18 号8
ファイル
コンテンツ更新日時 2026-02-18