FIG 4.

Elongasome function is critical for growth during LOS deficiency. (A) LOS-deficient mutants were rare in 5075 Tn mutants that disrupted the elongasome and quickly picked up the suppressor to stabilize the OM. Selections for LOS-deficient mutants were performed with 10 μg/ml of polymyxin B in 10 biological replicates per strain. (B) Tabular summary of mutations not found in the indicated strains isogenic parent shows that LOS/elongasome-deficient mutants quickly picked up suppressor mutations that predominantly disrupted mla genes, pldA, or both. (C) Doubling times from triplicate cultures of isolated LOS-deficient mutants. Since most LOS/elongasome-deficient mutants gained suppressor mutations in mla or pldA genes, growth rates were compared to a 5075 LOS-deficient suppressor that also inactivated mlaD. Above, average doubling times and significant differences, assessed as indicated in the Materials and Methods; *, P ≤ 0.05; **, P ≤ 0.01; ***, P ≤ 0.001; ****, P ≤ 0.0001.