Figure 4.

Effects of the new divIVA mutations on protein stability, sporulation, and control of MinCD function. (A) Western blot analysis of protein accumulation in sporulating cells of the divIVA null mutant 3011 (lane 1), the wild-type control 3012 (lane 2), 3013 (N99D; lane 3), 3015 (promoter mutation; lane 4), and 3016 (L140F; lane 5), taken at t₂₁₀. (B) Alkaline phosphatase synthesis during sporulation in strains 3011 (divIVA::cat, ▴), 3012 (divIVA⁺, ▪), 3013 (N99D, ▵), and 3014 (V25I, □). (C–F) Cell division and chromosome segregation in the 3017 mutant. Strain 3017, bearing the mutant divIVA allele conferring the N99D substitution, was induced to sporulate, and samples taken before resuspension (i.e., in CH growth medium; C,D) and 85 min after initiation of sporulation (E,F) were stained and visualized for the cell membrane (with FM5–95; C,E) and for DNA (with DAPI; D,F). Arrows in panels E and F point to the positions of some prespore compartments visible with the membrane stain, some of which are clearly deficient in DNA.