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. Author manuscript; available in PMC: 2017 Feb 11.
Published in final edited form as: Cell. 2016 Feb 4;164(4):710–721. doi: 10.1016/j.cell.2015.12.053

Figure 4. Degradation of phage transcripts by Csm3 and Csm6 enables type III CRISPR-Cas immunity targeting late-expressed genes.

Figure 4

(A) Staphylococci harboring different type III-A CRISPR-Cas systems targeting the gp14 gene were grown in liquid media and infected with ϕNM1γ6 phage (at 0 hours) with a multiplicity of infection of 5 viruses per bacteria. Optical density at 600 nm (OD600) was measured for the following 12 hours to monitor cell survival due to CRISPR immunity against the phage. Representative growth curves of at least three independent assays are shown. (B) Same as panel (A) but with the CRISPR-Cas systems programmed to target gp43. (C) The different infections performed in panel (A) were plated to enumerate plaque forming units (pfu) and calculate the average burst size. Mean ± S.D. of three replicas are reported. (D) Same as panel (C) but with the CRISPR-Cas systems programmed to target gp43. (E) Survival of cells (determined by measuring growth at OD600) carrying dcsm6/dcsm3 type III-A CRISPR-Cas systems targeting the different ϕNM1γ6 genes shown in Fig. 2A. Representative growth curves of at least three independent assays are shown.