Skip to main content
. Author manuscript; available in PMC: 2021 May 6.
Published in final edited form as: Nat Chem Biol. 2020 Dec 16;17(1):10–19. doi: 10.1038/s41589-020-00700-7

Table 2.

Summary of known Anti-CRISPR mechanisms

Regulator Acr type Key Mechanism
AcrF120 Competitive - Blocks dsDNA binding by interacting with Cas7f
AcrF220 - Blocks dsDNA binding by wedging between Cas8f and Cas7.6f
AcrF322 - Interacts with Cas3 and blocks its interaction with Csy complex
AcrF10100 - Blocks dsDNA binding by making contacts with Cas5f, 7f and 8f.

AcrIIA225 Competitive - Blocks dsDNA by interacting with PAM interaction sites on Cas9
AcrIIA426 - Blocks dsDNA by interacting with PAM interaction sites on Cas9
AcrIIC123 - Inhibits catalytic activity of Cas9 by interacting with the HNH domain
AcrIIC224 - Interacts with the bridge-helix region of Cas9 and blocks guide RNA binding

AcrVIA127,72 Competitive - Blocks target RNA binding by interacting with the crRNA, Helical-1, NTD, HEPN-1, and Linker domains of Cas13a-crRNA complex

AcrIIA628 Allosteric - Interacts as a dimer with the Cas9-sgRNA complex formed by WED and PAM-interacting domain reducing target DNA binding.
AcrIIC323 - Interacts as a dimer with non-catalytic sites of HNH and dimerizes Cas9 to prevent dsDNA binding

AcrVA429 Allosteric - Interacts as a dimer with Cas12a at the WED and bridge-helix to prevent stable dsDNA interaction.

AcrIII133 Enzymatic - Degrades cOAs through its ring nuclease activity

AcrVA131 Enzymatic - Occupies PAM binding groove on Cas12a-crRNA complex and endoribonucleolytically cleaves crRNA
AcrVA532 - Acetylates Lys635 on Cas12a and prevents dsDNA binding