Figure 2.
Inactivation of prc or nlpI suppresses the synthetic lethality between mepS and mepM mutations. (A) A diagram of the transposon insertion sites of suppressors isolated from the selection of a random transposon insertion library of HC611 (Para::mepS, ΔmepM) on LB agar. The triangles above the gene arrow represent the insertion for which the direction of transcription in the kanamycin resistance cassette of the transposon is in the same orientation as the disrupted gene; the triangles below, the opposite direction. (B) MG1655, HC611, and the Δprc and ΔnlpI derivative strains of HC611 grown overnight in M9-arabinose medium were serially diluted in LB and spotted onto LB agar. The plates were incubated at 30°C and photographed after 22 h for comparison of growth phenotype. (C) MG1655, WJ310 (ΔmepS ΔmepM), WJ323 (ΔmepS ΔmepM Δprc), and WJ324 (ΔmepS ΔmepM ΔnlpI) grown overnight in M9-glucose minimal medium lacking casamino acids were diluted, spotted, incubated, and imaged in the same way as in (B).