FIG 2.

ftsA point mutants can delay or exacerbate ΔCTL-induced bulging, filamentation, and lysis. (A to E) Phase-contrast, epifluorescence, and merged images of cells with ftsA WT (A), ftsA^R195C (B), ftsA^A295M (C), ftsA^I161F (D), or ftsA^R371A (E) as the only copy of ftsA uninduced with glucose or induced with xylose to drive expression of ΔCTL from P_xylX promoter for indicated amounts of time prior to imaging. White arrowheads indicate cells with nearly complete constriction, resulting in a chaining morphology. Red arrowheads indicate bulges that are asymmetric about the long axis of the cell. Yellow arrowheads indicate regions of hypercurvature. (F) Growth characteristics of cells shown in panel A, uninduced (closed circles) or induced (open circles) for ΔCTL expression, represented as absorbance at OD₆₀₀ over time. Shaded regions represent standard deviations of three technical replicates at each point. (G) Spot dilutions of strains shown in panel A showing growth of cells uninduced with glucose or induced with xylose (+ΔCTL) for ΔCTL expression. Cells in log phase were diluted to an OD₆₀₀ of 0.05, serially diluted, and spotted onto PYE agar plates with indicated inducer (glucose or xylose). Plates were incubated at 30°C for 48 h before imaging. (H) Immunoblot using anti-FtsZ antibody showing protein levels of ΔCTL and WT FtsZ corresponding to the experiments shown in panel A at 6.5 h of incubation with xylose. Strains are as indicated, and all strains have xylose-inducible ΔCTL.