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Human DNA helicase HELQ participates in DNA interstrand crosslink tolerance with ATR and RAD51 paralogs

Author

Listed:
  • Kei-ichi Takata

    (The University of Texas MD Anderson Cancer Center Science Park)

  • Shelley Reh

    (The University of Texas MD Anderson Cancer Center Science Park)

  • Junya Tomida

    (The University of Texas MD Anderson Cancer Center Science Park)

  • Maria D. Person

    (ICMB Protein and Metabolite Analysis Facility, University of Texas at Austin)

  • Richard D. Wood

    (The University of Texas MD Anderson Cancer Center Science Park
    Graduate School of Biomedical Sciences at Houston)

Abstract

Mammalian HELQ is a 3′–5′ DNA helicase with strand displacement activity. Here we show that HELQ participates in a pathway of resistance to DNA interstrand crosslinks (ICLs). Genetic disruption of HELQ in human cells enhances cellular sensitivity and chromosome radial formation by the ICL-inducing agent mitomycin C (MMC). A significant fraction of MMC sensitivity is independent of the Fanconi anaemia pathway. Sister chromatid exchange frequency and sensitivity to UV radiation or topoisomerase inhibitors is unaltered. Proteomic analysis reveals that HELQ is associated with the RAD51 paralogs RAD51B/C/D and XRCC2, and with the DNA damage-responsive kinase ATR. After treatment with MMC, reduced phosphorylation of the ATR substrate CHK1 occurs in HELQ-knockout cells, and accumulation of G2/M cells is reduced. The results indicate that HELQ operates in an arm of DNA repair and signalling in response to ICL. Further, the association with RAD51 paralogs suggests HELQ as a candidate ovarian cancer gene.

Suggested Citation

  • Kei-ichi Takata & Shelley Reh & Junya Tomida & Maria D. Person & Richard D. Wood, 2013. "Human DNA helicase HELQ participates in DNA interstrand crosslink tolerance with ATR and RAD51 paralogs," Nature Communications, Nature, vol. 4(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3338
    DOI: 10.1038/ncomms3338
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    Cited by:

    1. Sean West & Sushil Kumar & Surinder K Batra & Hesham Ali & Dario Ghersi, 2019. "Uncovering and characterizing splice variants associated with survival in lung cancer patients," PLOS Computational Biology, Public Library of Science, vol. 15(10), pages 1-16, October.
    2. Jiexiang Zhao & Ping Lu & Cong Wan & Yaping Huang & Manman Cui & Xinyan Yang & Yuqiong Hu & Yi Zheng & Ji Dong & Mei Wang & Shu Zhang & Zhaoting Liu & Shuhui Bian & Xiaoman Wang & Rui Wang & Shaofang , 2021. "Cell-fate transition and determination analysis of mouse male germ cells throughout development," Nature Communications, Nature, vol. 12(1), pages 1-20, December.
    3. Jessica D. Tischler & Hiroshi Tsuchida & Rosevalentine Bosire & Tommy T. Oda & Ana Park & Richard O. Adeyemi, 2024. "FLIP(C1orf112)-FIGNL1 complex regulates RAD51 chromatin association to promote viability after replication stress," Nature Communications, Nature, vol. 15(1), pages 1-18, December.
    4. J. A. Kamp & B. B. L. G. Lemmens & R. J. Romeijn & S. C. Changoer & R. Schendel & M. Tijsterman, 2021. "Helicase Q promotes homology-driven DNA double-strand break repair and prevents tandem duplications," Nature Communications, Nature, vol. 12(1), pages 1-12, December.

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