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

Niek Wietmarschen, Sarra Merzouk, Nancy Halsema, Diana C. J. Spierings, Victor Guryev and Peter M. Lansdorp ()
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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

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-017-02760-1

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