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Prophages are associated with extensive CRISPR-Cas auto-immunity

View ORCID ProfileFranklin L. Nobrega, Hielke Walinga, Bas E. Dutilh, Stan J.J. Brouns
doi: https://doi.org/10.1101/2020.03.02.973784
Franklin L. Nobrega
1Department of Bionanoscience, Delft University of Technology, Delft, Netherlands
2Kavli Institute of Nanoscience, Delft, Netherlands
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  • ORCID record for Franklin L. Nobrega
Hielke Walinga
1Department of Bionanoscience, Delft University of Technology, Delft, Netherlands
2Kavli Institute of Nanoscience, Delft, Netherlands
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Bas E. Dutilh
3Theoretical Biology and Bioinformatics, Science4Life, Utrecht University, Utrecht, Netherlands
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  • For correspondence: stanbrouns@gmail.com bedutilh@gmail.com
Stan J.J. Brouns
1Department of Bionanoscience, Delft University of Technology, Delft, Netherlands
2Kavli Institute of Nanoscience, Delft, Netherlands
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  • For correspondence: stanbrouns@gmail.com bedutilh@gmail.com
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ABSTRACT

CRISPR-Cas systems require discriminating self from non-self DNA during adaptation and interference. Yet, multiple cases have been reported of bacteria containing self-targeting spacers (STS), i.e. CRISPR spacers targeting protospacers on the same genome. STS has been suggested to reflect potential auto-immunity as an unwanted side effect of CRISPR-Cas defense, or a regulatory mechanism for gene expression. Here we investigated the incidence, distribution, and evasion of STS in over 100,000 bacterial genomes. We found STS in all CRISPR-Cas types and in one fifth of all CRISPR-carrying bacteria. Notably, up to 40% of I-B and I-F CRISPR-Cas systems contained STS. We observed that STS-containing genomes almost always carry a prophage and that STS map to prophage regions in more than half of the cases. Despite carrying STS, genetic deterioration of CRISPR-Cas systems appears to be rare, suggesting a level of escape from the potentially deleterious effects of STS by other mechanisms such as anti-CRISPR proteins and CRISPR target mutations. We propose a scenario where it is common to acquire an STS against a prophage, and this may trigger more extensive STS buildup by primed spacer acquisition in type I systems, without detrimental autoimmunity effects. The mechanisms of auto-immunity evasion create tolerance to STS-targeted prophages, and contribute both to viral dissemination and bacterial diversification.

Competing Interest Statement

The authors have declared no competing interest.

Footnotes

  • https://github.com/hwalinga/self-targeting-spacers-scripts

  • https://github.com/hwalinga/self-targeting-spacers-notebooks

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted August 04, 2020.
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Prophages are associated with extensive CRISPR-Cas auto-immunity
Franklin L. Nobrega, Hielke Walinga, Bas E. Dutilh, Stan J.J. Brouns
bioRxiv 2020.03.02.973784; doi: https://doi.org/10.1101/2020.03.02.973784
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Prophages are associated with extensive CRISPR-Cas auto-immunity
Franklin L. Nobrega, Hielke Walinga, Bas E. Dutilh, Stan J.J. Brouns
bioRxiv 2020.03.02.973784; doi: https://doi.org/10.1101/2020.03.02.973784

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