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TDP1-independent pathways in the process and repair of TOP1-induced DNA damage

Author

Listed:
  • Huimin Zhang

    (The University of Texas MD Anderson Cancer Center)

  • Yun Xiong

    (The University of Texas MD Anderson Cancer Center)

  • Dan Su

    (The University of Texas MD Anderson Cancer Center)

  • Chao Wang

    (The University of Texas MD Anderson Cancer Center)

  • Mrinal Srivastava

    (The University of Texas MD Anderson Cancer Center)

  • Mengfan Tang

    (The University of Texas MD Anderson Cancer Center)

  • Xu Feng

    (The University of Texas MD Anderson Cancer Center)

  • Min Huang

    (The University of Texas MD Anderson Cancer Center)

  • Zhen Chen

    (The University of Texas MD Anderson Cancer Center)

  • Junjie Chen

    (The University of Texas MD Anderson Cancer Center)

Abstract

Anticancer drugs, such as camptothecin (CPT), trap topoisomerase I (TOP1) on DNA and form TOP1 cleavage complexes (TOP1cc). Alternative repair pathways have been suggested in the repair of TOP1cc. However, how these pathways work with TDP1, a key repair enzyme that specifically hydrolyze the covalent bond between TOP1 catalytic tyrosine and the 3’-end of DNA and contribute to the repair of TOP1cc is poorly understood. Here, using unbiased whole-genome CRISPR screens and generation of co-deficient cells with TDP1 and other genes, we demonstrate that MUS81 is an important factor that mediates the generation of excess double-strand breaks (DSBs) in TDP1 KO cells. APEX1/2 are synthetic lethal with TDP1. However, deficiency of APEX1/2 does not reduce DSB formation in TDP1 KO cells. Together, our data suggest that TOP1cc can be either resolved directly by TDP1 or be converted into DSBs and repaired further by the Homologous Recombination (HR) pathway.

Suggested Citation

  • Huimin Zhang & Yun Xiong & Dan Su & Chao Wang & Mrinal Srivastava & Mengfan Tang & Xu Feng & Min Huang & Zhen Chen & Junjie Chen, 2022. "TDP1-independent pathways in the process and repair of TOP1-induced DNA damage," Nature Communications, Nature, vol. 13(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-31801-7
    DOI: 10.1038/s41467-022-31801-7
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    References listed on IDEAS

    as
    1. Xiao Wu & Bin Wang, 2021. "Abraxas suppresses DNA end resection and limits break-induced replication by controlling SLX4/MUS81 chromatin loading in response to TOP1 inhibitor-induced DNA damage," Nature Communications, Nature, vol. 12(1), pages 1-15, December.
    2. Christopher J. Bakkenist & Michael B. Kastan, 2003. "DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation," Nature, Nature, vol. 421(6922), pages 499-506, January.
    3. Pauline Chanut & Sébastien Britton & Julia Coates & Stephen P. Jackson & Patrick Calsou, 2016. "Coordinated nuclease activities counteract Ku at single-ended DNA double-strand breaks," Nature Communications, Nature, vol. 7(1), pages 1-12, November.
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    Cited by:

    1. Diana Rubio-Contreras & Fernando Gómez-Herreros, 2023. "TDP1 suppresses chromosomal translocations and cell death induced by abortive TOP1 activity during gene transcription," Nature Communications, Nature, vol. 14(1), pages 1-14, December.

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