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ZFP161 regulates replication fork stability and maintenance of genomic stability by recruiting the ATR/ATRIP complex

Author

Listed:
  • Wootae Kim

    (Mayo Clinic
    Mayo Clinic)

  • Fei Zhao

    (Mayo Clinic
    Mayo Clinic)

  • Rentian Wu

    (Mayo Clinic
    Mayo Clinic)

  • Sisi Qin

    (Mayo Clinic)

  • Somaira Nowsheen

    (Mayo Clinic
    Mayo Clinic
    Mayo Clinic)

  • Jinzhou Huang

    (Mayo Clinic
    Mayo Clinic)

  • Qin Zhou

    (Mayo Clinic
    Mayo Clinic)

  • Yuping Chen

    (Tongji University School of Medicine
    Tongji University School of Medicine)

  • Min Deng

    (Mayo Clinic
    Mayo Clinic)

  • Guijie Guo

    (Mayo Clinic
    Mayo Clinic)

  • Kuntian Luo

    (Mayo Clinic
    Mayo Clinic)

  • Zhenkun Lou

    (Mayo Clinic
    Mayo Clinic)

  • Jian Yuan

    (Tongji University School of Medicine
    Tongji University School of Medicine)

Abstract

DNA replication stress-mediated activation of the ATR kinase pathway is important for maintaining genomic stability. In this study, we identified a zinc finger protein, ZFP161 that functions as a replication stress response factor in ATR activation. Mechanistically, ZFP161 acts as a scaffolding protein to facilitate the interaction between RPA and ATR/ATRIP. ZFP161 binds to RPA and ATR/ATRIP through distinct regions and stabilizes the RPA–ATR–ATRIP complex at stalled replication forks. This function of ZFP161 is important to the ATR signaling cascade and genome stability maintenance. In addition, ZFP161 knockout mice showed a defect in ATR activation and genomic instability. Furthermore, low expression of ZFP161 is associated with higher cancer risk and chromosomal instability. Overall, these findings suggest that ZFP161 coordinates ATR/Chk1 pathway activation and helps maintain genomic stability.

Suggested Citation

  • Wootae Kim & Fei Zhao & Rentian Wu & Sisi Qin & Somaira Nowsheen & Jinzhou Huang & Qin Zhou & Yuping Chen & Min Deng & Guijie Guo & Kuntian Luo & Zhenkun Lou & Jian Yuan, 2019. "ZFP161 regulates replication fork stability and maintenance of genomic stability by recruiting the ATR/ATRIP complex," Nature Communications, Nature, vol. 10(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-13321-z
    DOI: 10.1038/s41467-019-13321-z
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