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Inhibition of NHEJ repair by type II-A CRISPR-Cas systems in bacteria

Author

Listed:
  • Aude Bernheim

    (Microbial Evolutionary Genomics, Institut Pasteur
    CNRS, UMR3525
    Synthetic Biology Group, Institut Pasteur
    AgroParisTech)

  • Alicia Calvo-Villamañán

    (Synthetic Biology Group, Institut Pasteur)

  • Clovis Basier

    (Synthetic Biology Group, Institut Pasteur)

  • Lun Cui

    (Synthetic Biology Group, Institut Pasteur)

  • Eduardo P. C. Rocha

    (Microbial Evolutionary Genomics, Institut Pasteur
    CNRS, UMR3525)

  • Marie Touchon

    (Microbial Evolutionary Genomics, Institut Pasteur
    CNRS, UMR3525)

  • David Bikard

    (Synthetic Biology Group, Institut Pasteur)

Abstract

Type II CRISPR-Cas systems introduce double-strand breaks into DNA of invading genetic material and use DNA fragments to acquire novel spacers during adaptation. These breaks can be the substrate of several DNA repair pathways, paving the way for interactions. We report that non-homologous end-joining (NHEJ) and type II-A CRISPR-Cas systems only co-occur once among 5563 fully sequenced prokaryotic genomes. We investigated experimentally the possible molecular interactions using the NHEJ pathway from Bacillus subtilis and the type II-A CRISPR-Cas systems from Streptococcus thermophilus and Streptococcus pyogenes. Our results suggest that the NHEJ system has no effect on CRISPR immunity. On the other hand, we provide evidence for the inhibition of NHEJ repair by the Csn2 protein. Our findings give insights on the complex interactions between CRISPR-Cas systems and repair mechanisms in bacteria, contributing to explain the scattered distribution of CRISPR-Cas systems in bacterial genome.

Suggested Citation

  • Aude Bernheim & Alicia Calvo-Villamañán & Clovis Basier & Lun Cui & Eduardo P. C. Rocha & Marie Touchon & David Bikard, 2017. "Inhibition of NHEJ repair by type II-A CRISPR-Cas systems in bacteria," Nature Communications, Nature, vol. 8(1), pages 1-9, December.
  • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-02350-1
    DOI: 10.1038/s41467-017-02350-1
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