SspA is a transcriptional regulator of CRISPR adaptation in <i>E. coli</i>
The CRISPR integrases Cas1-Cas2 create immunological memories of viral infection by storing phage-derived DNA in CRISPR arrays, a process known as CRISPR adaptation. A number of host factors have been shown to influence adaptation, but the full pathway from infection to a fully integrated, phage-derived sequences in the array remains incomplete. Here, we deploy a new CRISPRi-based screen to identify putative host factors that participate in CRISPR adaptation in the Escherichia coli Type I-E system. Our screen and subsequent mechanistic characterization reveal that SspA, through its role as a global transcriptional regulator of cellular stress, is required for functional CRISPR adaptation. One target of SspA is H-NS, a known repressor of CRISPR interference proteins, but we find that the role of SspA on adaptation is not H-NS-dependent. We propose a new model of CRISPR-Cas defense that includes independent cellular control of adaptation and interference by SspA.
Authors
- Seth L. Shipman (ORCID: https://orcid.org/0000-0003-3130-8043)
- Santiago C. Lopez (ORCID: https://orcid.org/0000-0001-7576-2438)
- Yumie Lee
- Karen Zhang (ORCID: https://orcid.org/0000-0003-4406-9977)
Institutions
- Gladstone Institutes (US)
- University of California, San Francisco (US)
- Chan Zuckerberg Initiative (United States) (US)
Publication Details
- Journal
- Nucleic Acids Research
- Published
- 2024-12-27
- DOI
- https://doi.org/10.1093/nar/gkae1244
- Citations
- 3
- Primary Topic
- CRISPR and Genetic Engineering
- Type
- article
- Field-Weighted Citation Impact
- 0.70
Funders
- National Science Foundation