Fig 6 -

Qtip-mediated inactivation of cIVP882, and not RecA-mediated cIVP882proteolysis, is required for host QS control of phage VP882 gene expression. (A) SDS-PAGE in-gel labeling of HALO-cIVP882 produced from a plasmid in the indicated strains.–and + indicate, respectively, the absence and presence of ciprofloxacin to induce SOS. The FL and scissors labels designate full-length and cleaved cIVP882 proteins, respectively. M denotes the molecular weight marker. kDa is kilodaltons. (B) Relative Pgp69-lux output in the indicated recA+ (black bars) and ΔrecA (white bars) 882 strains. (C) Growth of ΔrecA strain 882 (cyan), ΔrecA 882 vqmR-vqmA882+ (green), ΔrecA 882 luxO+ (orange), and ΔrecA 882 vqmR-vqmA882+ luxO+ (red) strains carrying arabinose-inducible vqmAPhage and grown in medium lacking (diamonds) or containing (circles) 0.02% arabinose. (D) As in (B), except with strains carrying either phage VP882 Ctr::cm (black bars) or phage VP882 qtip::cm (white bars). All strains are recA+. (E) As in (B), except with strains carrying either VP882* or VP882* ΔvqmAPhage-qtip. Data are represented as means ± std with n = 3 biological replicates (B, C, D, E), and as representative of three independent experiments (A). RLU as in Fig 2B (B, D, E).