Fig. 2
PhrS stimulates CRISPR2 crRNA transcription and subsequent CRISPR-Cas interference. a cas-lacZ or CRISPR-lacZ activity in PA14 WT and ΔphrS mutant backgrounds throughout the growth period. b Transformation efficiency with CR1-sp1 and CR2-sp1 plasmids in PA14 WT or ΔphrS mutant. c Phage plaque assay of JBD18 and JBD25 for PA14 WT, ΔphrS, ΔphrS/p-phrS, and PA14 lacking a CRISPR-Cas system (ΔTCR). d Northern blot of crRNA levels, PhrS, and 5S RNA in PA14 WT and its mutant strains. e Retention of the CRISPR-targeted plasmid CR2-sp1 in the PA14 ΔphrS background strain with pgRNA-CRISPR2 that coexpressed the crRNA in the CRISPR2 locus. f Transformation efficiency of CR2-sp1 vector in PA14 ΔphrS background strain with pgRNA-CRISPR2. g The same JBD18 phage was tested on PA14 ΔphrS background strain containing pgRNA empty vector or plasmid expression the indicated CRISPR2. Results are shown with mean ± SEM from three independent experiments. **P < 0.01, *P < 0.05, one-way ANOVA plus Tukey test
