Type III CRISPR-Cas systems can provide redundancy to counteract viral escape from type I systems
Abstract
CRISPR-Cas-mediated defense utilizes information stored as spacers in CRISPR arrays to defend against genetic invaders. We define the mode of target interference and role in antiviral defense for two CRISPR-Cas systems in Marinomonas mediterranea. One system (type I-F) targets DNA. A second system (type III-B) is broadly capable of acquiring spacers in either orientation from RNA and DNA, and exhibits transcription-dependent DNA interference. Examining resistance to phages isolated from Mediterranean seagrass meadows, we found that the type III-B machinery co-opts type I-F CRISPR-RNAs. Sequencing and infectivity assessments of related bacterial and phage strains suggests an "arms race" in which phage escape from the type I-F system can be overcome through use of type I-F spacers by a horizontally-acquired type III-B system. We propose that the phage-host arms race can drive selection for horizontal uptake and maintenance of promiscuous type III interference modules that supplement existing host type I CRISPR-Cas systems.
Data availability
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CRISPR targeting and spacer acquisition in M. mediterranea mutants, and associated environmental investigationsPublicly accessible at NCBI Sequence Read Archive (accession no. SRP103952).
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total RNA (> 200 nt) sequencing from MMB-1 strains over-expressing RT-Cas1, Cas2, and Marme_0670 - replicate 1Publicly accessible at NCBI Sequence Read Archive (accession no. SRR2914032).
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total RNA (> 200 nt) sequencing from MMB-1 strains over-expressing RT-Cas1, Cas2, and Marme_0670 - replicate 2Publicly accessible at NCBI Sequence Read Archive (accession no. SRR2914033).
Article and author information
Author details
Funding
National Institutes of Health (R01-GM37706)
- Andrew Z Fire
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Blake Wiedenheft, Montana State University, United States
Version history
- Received: April 8, 2017
- Accepted: August 7, 2017
- Accepted Manuscript published: August 17, 2017 (version 1)
- Version of Record published: August 30, 2017 (version 2)
- Version of Record updated: March 2, 2018 (version 3)
- Version of Record updated: April 4, 2018 (version 4)
Copyright
© 2017, Silas et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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Further reading
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- Microbiology and Infectious Disease
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