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. 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

Figure 5. Fine tuning type III CRISPR-Cas immunity.

Figure 5.

Schematic showing the type III CRISPR mechanism and the role of accessory nucleases in controlling type III immunity. The type III CRISPR-Cas pathway involves targeting of RNA by the Csm/Cmr complex during transcription followed by the activation of Cas10 that results in cleavage of DNA and the production of cOAs. The cOAs released by Cas10 then activates the accessory nuclease Csm6/Csx1 which then leads to non-specific cleavage of RNA. This second messenger pathway can further be supplemented by other accessory RNA-targeting nucleases, RNaseJ1/J2 and PNPase and DNA targeting nucleases including NucC and Can1 that can cleave dsDNA and ssDNA, respectively. The concentration of the cOA molecules can be controlled both by the host ring nucleases (Crn1–3) and MGE-derived ring nuclease (AcrIII-I)