Figure 9. λ lysogen induction inhibits host cell division in a kil-dependent manner.

(A) Induction of a λ lysogen results in a kil-dependent increase in E. coli cell length prior to host cell lysis. The average fixed-cell lengths of indicated kil⁺ and kil⁻ strain populations 40 minutes post λ lysogen induction (42°C), or control non-inducing conditions (30°C) are plotted. Error bars represent standard deviation between three separate population measurements. (B) Induction of a λ lysogen results in a kil-dependent, near-total ablation of FtsZ rings prior to host lysis. Representative IFM micrographs stained for cell wall (red) and α-FtsZ (green) are shown from the same fixed cells used for (A); the indicated genotypes and growth temperatures are listed. Cell wall and α-FtsZ signals are as described in Figure 2. Scale bar = 5 µm. (C) A one-step growth curve of kil⁺ phage (solid circles) and kil⁻ phage (open circles) showing plaque forming units (pfu) per mL over time in MG1655 at 39°C. (D) A model (with key to shapes on right) for Kil activity on FtsZ ring formation (top cartoons) is depicted for the indicated strain genotypes, and the resulting effects on cellular phenotype (lower cartoons). The top left cartoon illustrates the kil⁻ condition alone, not all Kil-resistant conditions. The recruitment of Kil to midcell inhibits FtsZ assembly by completely blocking normal FtsZ ring assembly. FtsZ blobs and spirals seen by IFM suggest that FtsZ assembles aberrantly in the presence of Kil in vivo, unable to resolve into a closed ring structure. See discussion for the potential role of ZipA. Cell filamentation may increase lysis time in an un-compartmentalized host.