TABLE 6.
Effect of ScoC on expression of CodY-regulated fusionsa
| Strain | Fusion promoter | Relevant genotype | β-Galactosidase activity (Miller units) |
|---|---|---|---|
| BB3654 | ispA-lacZ | Wild type | 0.11 |
| BB3875 | scoC | 0.17 | |
| BB3659 | codY | 12.3 | |
| BB3879 | codY scoC | 14.1 | |
| BB3550 | hutP-lacZ | Wild type | 0.45 |
| BB3873 | scoC | 0.48 | |
| BB3899 | codY | 9.32 | |
| BB3900 | codY scoC | 9.91 | |
| BB2781 | dppA-lacZ | abrB | 6.28 |
| BB3921 | scoC abrB | 5.42 | |
| BB2786 | codY abrB | 373.8 | |
| BB3922 | codY scoC abrB | 249.8 | |
| BB2770 | ybgE292-lacZ | Wild type | 1.12 |
| BB3918 | scoC | 1.05 | |
| BB2771 | codY | 427.8 | |
| BB4089 | codY scoC | 442.0 |
a
Cells were grown and β-galactosidase specific activity was assayed as described in the footnote to Table 3. Histidine (0.1%) was added to the medium in experiments with the hutP-lacZ fusion to induce promoter expression. The dppA-lacZ fusion was tested in abrB mutant cells to abolish AbrB-mediated repression of the dppA promoter (35). The activity of endogenous β-galactosidase was ≤0.05 Miller unit.