TABLE 3.
Strain | Plasmid (gene)a | GFP intensity (geometric mean ± SD)b |
||
---|---|---|---|---|
HMM | HMM + 0.1 mM SHX | HMM + 0.5% αMG | ||
Ea1189 | pFPV25 | 1.34 ± 0.021e | 1.35 ± 0.007e | 1.36 ± 0.014d |
pZW2 (hrpL) | 1.58 ± 0.035c,d | 1.54 ± 0.007c,d | 1.52 ± 0.014c | |
ΔrelA mutant | pZW2 (hrpL) | 1.47 ± 0.007c,d | 1.42 ± 0.021d | 1.41 ± 0.022c |
ΔspoT mutant | pZW2 (hrpL) | 2.3 ± 0.028b | 2.64 ± 0.233b | 5.15 ± 0.234b |
Ea1189 | pHrpA-GFP | 1.72 ± 0.049c | 1.93 ± 0.035c | 1.98 ± 0.036c |
ΔrelA mutant | pHrpA-GFP | 1.42 ± 0.021d | 1.49 ± 0.14c,d | 1.44 ± 0.15c |
ΔspoT mutant | pHrpA-GFP | 3.55 ± 0.355a | 5.98 ± 0.63a | 13.94 ± 0.96a |
Promoter-GFP fusion plasmid.
Bacteria were grown in HMM for 18 h, with or without addition of serine hydroxamate (SHX) or α-methylglucoside (αMG). One-way ANOVA and Student's t test (P = 0.05) were used to analyze the data. GFP intensity values within a treatment marked with the same letter were not significantly different (P < 0.05).