Table 2.
Regulation of the promoters of bcam0191 and bcam0192 by CepR2, CepS, and OHL.
| Fusiona | Chromosomal genotypeb | Plasmid genotype | OHL (uM) | β-Galactosidase | Normalized Valuesc |
|---|---|---|---|---|---|
| bcam0191 | WT | none | 0 | 35 ± 8 | (1) |
| WT | none | 1 | 377 ± 30 | 10.8 | |
| GR141 (cepR2-) | pSRKKm | 0 | 383 ± 24 | 10.9 | |
| GR141 (cepR2-) | pSRKKm | 1 | 397 ± 32 | 11.3 | |
| GR141 (cepR2-) | pGR192 (cepR2) | 0 | 33 ± 4 | 0.95 | |
| GR141 (cepR2-) | pGR192 (cepR2) | 1 | 387 ± 21 | 11.1 | |
| GR145 (cepS-) | pSRKGm | 0 | 5 ± 3 | 0.14 | |
| GR145 (cepS-) | pSRKGm | 1 | 3 ± 2 | 0.1 | |
| GR145 (cepS-) | pGR193 (cepS) | 0 | 41 ± 8 | 1.2 | |
| GR145 (cepS-) | pGR193 (cepS) | 1 | 412 ± 32 | 11.8 | |
| bcam0192 | WT | none | 0 | 32 ± 3 | (1) |
| WT | none | 1 | 362 ± 15 | 11.3 | |
| GR141 (cepR2-) | pSRKKm | 0 | 376 ± 31 | 11.8 | |
| GR141 (cepR2-) | pSRKKm | 1 | 368 ± 25 | 11.5 | |
| GR141 (cepR2-) | pGR192 (cepR2) | 0 | 36 ± 1 | 1.1 | |
| GR141 (cepR2-) | pGR192 (cepR2) | 1 | 373 ± 24 | 11.7 | |
| GR145 (cepS-) | pSRKGm | 0 | 3 ± 1 | 0.1 | |
| GR145 (cepS-) | pSRKGm | 1 | 4 ± 2 | 0.13 | |
| GR145 (cepS-) | pGR193 (cepS) | 0 | 43 ± 1 | 1.3 | |
| GR145 (cepS-) | pGR193 (cepS) | 1 | 396 ± 36 | 12.4 |
A bcam0191-lacZ transcriptional fusion was provided by pGR130, while a bcam0192-lacZ fusion was provided using pGR136. The vector for both plasmids, pYW302, expressed only 1–2 units of β-galactosidase activity.
All strains are derived from K56-I2, which carries an insertion mutation in cepI. Strains were cultured at 37°C in LB supplemented with 0.5 mM IPTG, appropriate antibiotics, and containing or lacking OHL as indicated, to an OD600 of 0.4, and assayed for β-galactosidase activity. Data were obtained from a single representative experiment using three independent isolates of each strain, each assayed once. Mean value and standard deviations are indicated.
β-galactosidase activity is normalized to that of the wild type strain carrying the indicated plasmid and cultured in the absence of OHL.