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BLM helicase suppresses recombination at G-quadruplex motifs in transcribed genes

Author

Listed:
  • Niek Wietmarschen

    (University of Groningen, University Medical Center Groningen)

  • Sarra Merzouk

    (University of Groningen, University Medical Center Groningen)

  • Nancy Halsema

    (University of Groningen, University Medical Center Groningen)

  • Diana C. J. Spierings

    (University of Groningen, University Medical Center Groningen)

  • Victor Guryev

    (University of Groningen, University Medical Center Groningen)

  • Peter M. Lansdorp

    (University of Groningen, University Medical Center Groningen
    British Columbia Cancer Agency
    University of British Columbia)

Abstract

Bloom syndrome is a cancer predisposition disorder caused by mutations in the BLM helicase gene. Cells from persons with Bloom syndrome exhibit striking genomic instability characterized by excessive sister chromatid exchange events (SCEs). We applied single-cell DNA template strand sequencing (Strand-seq) to map the genomic locations of SCEs. Our results show that in the absence of BLM, SCEs in human and murine cells do not occur randomly throughout the genome but are strikingly enriched at coding regions, specifically at sites of guanine quadruplex (G4) motifs in transcribed genes. We propose that BLM protects against genome instability by suppressing recombination at sites of G4 structures, particularly in transcribed regions of the genome.

Suggested Citation

  • Niek Wietmarschen & Sarra Merzouk & Nancy Halsema & Diana C. J. Spierings & Victor Guryev & Peter M. Lansdorp, 2018. "BLM helicase suppresses recombination at G-quadruplex motifs in transcribed genes," Nature Communications, Nature, vol. 9(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-017-02760-1
    DOI: 10.1038/s41467-017-02760-1
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    Cited by:

    1. Anne Margriet Heijink & Colin Stok & David Porubsky & Eleni Maria Manolika & Jurrian K. Kanter & Yannick P. Kok & Marieke Everts & H. Rudolf Boer & Anastasia Audrey & Femke J. Bakker & Elles Wierenga , 2022. "Sister chromatid exchanges induced by perturbed replication can form independently of BRCA1, BRCA2 and RAD51," Nature Communications, Nature, vol. 13(1), pages 1-16, December.
    2. S. Cohen & A. Guenolé & I. Lazar & A. Marnef & T. Clouaire & D. V. Vernekar & N. Puget & V. Rocher & C. Arnould & M. Aguirrebengoa & M. Genais & N. Firmin & R. A. Shamanna & R. Mourad & V. A. Bohr & V, 2022. "A POLD3/BLM dependent pathway handles DSBs in transcribed chromatin upon excessive RNA:DNA hybrid accumulation," Nature Communications, Nature, vol. 13(1), pages 1-15, December.
    3. Timothy K. Turkalo & Antonio Maffia & Johannes J. Schabort & Samuel G. Regalado & Mital Bhakta & Marco Blanchette & Diana C. J. Spierings & Peter M. Lansdorp & Dirk Hockemeyer, 2023. "A non-genetic switch triggers alternative telomere lengthening and cellular immortalization in ATRX deficient cells," Nature Communications, Nature, vol. 14(1), pages 1-17, December.
    4. Chaoyou Xue & Sameer J. Salunkhe & Nozomi Tomimatsu & Ajinkya S. Kawale & Youngho Kwon & Sandeep Burma & Patrick Sung & Eric C. Greene, 2022. "Bloom helicase mediates formation of large single–stranded DNA loops during DNA end processing," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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