期刊
CELL
卷 168, 期 1-2, 页码 150-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2016.12.009
关键词
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资金
- University of California, San Francisco Program for Breakthrough in Biomedical Research
- Sandler Foundation
- NIH Office of the Director Early Independence Award [DP5-OD021344]
- National Science Foundation [1144247]
- Carol Gross' lab by Mira [R35GM118061]
- amFAR Mathilde Krim Fellowship [109504-61-RKRL]
- NIH Human Immunology Project Consortium Infrastructure Pilot [U19 AI118610]
- NIH [P30 AI027763]
- NIH HIV Accessory & Regulatory Complexes (HARC) Center [P50 GM082250]
Bacterial CRISPR-Cas systems utilize sequencespecific RNA-guided nucleases to defend against bacteriophage infection. As a countermeasure, numerous phages are known that produce proteins to block the function of class 1 CRISPR-Cas systems. However, currently no proteins are known to inhibit the widely used class 2 CRISPR-Cas9 system. To find these inhibitors, we searched cas9-containing bacterial genomes for the co-existence of a CRISPR spacer and its target, a potential indicator for CRISPR inhibition. This analysis led to the discovery of four unique type II-A CRISPR-Cas9 inhibitor proteins encoded by Listeria monocytogenes prophages. More than half of L. monocytogenes strains with cas9 contain at least one prophage-encoded inhibitor, suggesting widespread CRISPR-Cas9 inactivation. Two of these inhibitors also blocked the widely used Streptococcus pyogenes Cas9 when assayed in Escherichia coli and human cells. These natural Cas9-specific anti-CRISPRs'' present tools that can be used to regulate the genome engineering activities of CRISPR-Cas9.
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