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. 2016 Jan 15;198(3):394–409. doi: 10.1128/JB.00556-15

FIG 4.

FIG 4

GrvA represses gadE transcription through GadW, determined from β-galactosidase activity (in Miller units) for gadE-lacZ promoter fusions in TW14359 and genetic derivatives. (A) (Top) Activity (in Miller units) for gadE-lacZ promoter fragments Frag-1 through Frag-4 and the vector control (pRS551) plotted for TW14359 and TW14359 ΔgrvA during exponential-phase (OD600 = 0.5) and stationary-phase (OD600 = 2) growth in DMEM. (Bottom) Cartoon of the gadE promoter and flanking regions. Promoter (P1 to P3) positions and the positions of each cloned promoter fragment (Frag-1 through Frag-4) relative to position +1 of the initiation codon for the gadE ORF are indicated. (B) Activity (in Miller units) plotted for gadE-lacZ promoter fragments Frag-2 (left) and Frag-4 (right) in TW14359 and mutant derivatives. For panels A and B, asterisks denote significant differences by t test (n ≥ 3; *, P < 0.05; **, P < 0.01). Bars denote standard deviations. (C) Activity (in Miller units) plotted for the gadE-lacZ P3 promoter in TW14359 and mutant derivatives. Plots which differ by lowercase letter differ significantly by Tukey's HSD test following a significant F test (n ≥ 3, P < 0.05).