Display options
Cite
Garcia B, Lee J, Edraki A, et al. Anti-CRISPR AcrIIA5 Potently Inhibits All Cas9 Homologs Used for Genome Editing. Cell Rep. 2019;29(7):1739-1746.e5doi: 10.1016/j.celrep.2019.10.017.
Garcia, B., Lee, J., Edraki, A., Hidalgo-Reyes, Y., Erwood, S., Mir, A., Trost, C. N., Seroussi, U., Stanley, S. Y., Cohn, R. D., Claycomb, J. M., Sontheimer, E. J., Maxwell, K. L., & Davidson, A. R. (2019). Anti-CRISPR AcrIIA5 Potently Inhibits All Cas9 Homologs Used for Genome Editing. Cell reports, 29(7), 1739-1746.e5. https://doi.org/10.1016/j.celrep.2019.10.017
Garcia, Bianca, et al. "Anti-CRISPR AcrIIA5 Potently Inhibits All Cas9 Homologs Used for Genome Editing." Cell reports vol. 29,7 (2019): 1739-1746.e5. doi: https://doi.org/10.1016/j.celrep.2019.10.017
Garcia B, Lee J, Edraki A, Hidalgo-Reyes Y, Erwood S, Mir A, Trost CN, Seroussi U, Stanley SY, Cohn RD, Claycomb JM, Sontheimer EJ, Maxwell KL, Davidson AR. Anti-CRISPR AcrIIA5 Potently Inhibits All Cas9 Homologs Used for Genome Editing. Cell Rep. 2019 Nov 12;29(7):1739-1746.e5. doi: 10.1016/j.celrep.2019.10.017. PMID: 31722192; PMCID: PMC6910239.
Copy Download .nbib Format: NLM
Share it on

Cell Rep. 2019 Nov 12;29(7):1739-1746.e5. doi: 10.1016/j.celrep.2019.10.017.

Anti-CRISPR AcrIIA5 Potently Inhibits All Cas9 Homologs Used for Genome Editing.

Cell reports

Bianca Garcia, Jooyoung Lee, Alireza Edraki, Yurima Hidalgo-Reyes, Steven Erwood, Aamir Mir, Chantel N Trost, Uri Seroussi, Sabrina Y Stanley, Ronald D Cohn, Julie M Claycomb, Erik J Sontheimer, Karen L Maxwell, Alan R Davidson

Affiliations

  1. Department of Molecular Genetics, University of Toronto, Toronto, ON M5G 1M1, Canada.
  2. RNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA.
  3. Department of Molecular Genetics, University of Toronto, Toronto, ON M5G 1M1, Canada; Program in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.
  4. Department of Molecular Genetics, University of Toronto, Toronto, ON M5G 1M1, Canada; Program in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada; Department of Pediatrics, University of Toronto and The Hospital for Sick Children, Toronto, ON M5G 1X8, Canada.
  5. RNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA; Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
  6. Department of Biochemistry, University of Toronto, Toronto, ON M5G 1M1, Canada. Electronic address: [email protected].
  7. Department of Molecular Genetics, University of Toronto, Toronto, ON M5G 1M1, Canada; Department of Biochemistry, University of Toronto, Toronto, ON M5G 1M1, Canada. Electronic address: [email protected].

PMID: 31722192 PMCID: PMC6910239 DOI: 10.1016/j.celrep.2019.10.017

Abstract

CRISPR-Cas9 systems provide powerful tools for genome editing. However, optimal employment of this technology will require control of Cas9 activity so that the timing, tissue specificity, and accuracy of editing may be precisely modulated. Anti-CRISPR proteins, which are small, naturally occurring inhibitors of CRISPR-Cas systems, are well suited for this purpose. A number of anti-CRISPR proteins have been shown to potently inhibit subgroups of CRISPR-Cas9 systems, but their maximal inhibitory activity is generally restricted to specific Cas9 homologs. Since Cas9 homologs vary in important properties, differing Cas9s may be optimal for particular genome-editing applications. To facilitate the practical exploitation of multiple Cas9 homologs, here we identify one anti-CRISPR, called AcrIIA5, that potently inhibits nine diverse type II-A and type II-C Cas9 homologs, including those currently used for genome editing. We show that the activity of AcrIIA5 results in partial in vivo cleavage of a single-guide RNA (sgRNA), suggesting that its mechanism involves RNA interaction.

Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.

Keywords: Cas9; anti-CRISPR; bacteriophage; genome editing

Substances

MeSH terms

Publication Types

Grant support