Journal
MOLECULAR CELL
Volume 82, Issue 11, Pages 2161-+Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2022.05.002
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Funding
- UCSF Program for Breakthrough Biomedical Research - Sandler Foundation
- NIH [DP5-OD021344, R01GM127489, P01HL142494, R35GM142460]
- DARPA [HR0011-17-2-0043]
- NSF GRFP Fellowship
- Margaret Q. Landenberger Research Foundation
- Mass General Hospital Howard M. Goodman Fellowship
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This article questions the research findings of Lin et al. on CRISPR immunity and Acr proteins, highlighting inconsistencies in the study including inaccurate bioinformatics analyses and the impossibility of constructing certain bacterial strains.
CRISPR systems are prokaryotic adaptive immune systems that use RNA-guided Cas nucleases to recognize and destroy foreign genetic elements. To overcome CRISPR immunity, bacteriophages have evolved diverse families of anti-CRISPR proteins (Acrs). Recently, Lin et al. (2020) described the discovery and characterization of 7 Acr families (AcrVIA1-7) that inhibit type VI-A CRISPR systems. We detail several inconsistencies that question the results reported in the Lin et al. (2020) study. These include inaccurate bioinformatics analyses and bacterial strains that are impossible to construct. Published strains were provided by the authors, but MS2 bacteriophage plaque assays did not support the published results. We also independently tested the Acr sequences described in the original report, in E. coli and mammalian cells, but did not observe anti-Cas13a activity. Taken together, our data and analyses prompt us to question the claim that AcrVIA17 reported in Lin et al. are type VI anti-CRISPR proteins.
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