TABLE 3.
Control of the φKO2 gene 22 and 23 promoters by host LexA protein
| Relevant host genotypea | φKO2 promoter | β-Galactosidase activity (Miller units)b
|
|
|---|---|---|---|
| Without mitomycin C | With mitomycin C | ||
| UB-1548 (lexA+ sulA) | P22 | 27 | 672 |
| UB-1550 (lexA null sulA) | P22 | 1,962 | 2,610 |
| UB-1549 (lexA ind sulA) | P22 | 7 | 11 |
| UB-1547 (lexA ind sulA+) | P22 | 8 | 9 |
| UB-1555 (lexA+ sulA) | P23 | 2 | 68 |
| UB-1556 (lexA null sulA) | P23 | 219 | 187 |
| UB-1557 (lexA ind sulA) | P23 | 0.3 | 0.7 |
| UB-1558 (lexA ind sulA+) | P23 | 0.2 | 0.7 |
S. enterica LT2 lexA null mutants are lethal unless a sulA mutation is also present. All of these strains are cured of prophages Fels-2, Gifsy-1, and Gifsy-2, since these prophages can also interfere with the growth of lexA-negative strains (11). The lexA ind sulA+ strains are included to show that the sulA mutation does not cause SOS inducibility.
β-Galactosidase activity units show the change in A420 per minute per milliliter of cells per optical density unit at 600 nm. Cultures were grown with shaking at 37°C to an optical density at 600 nm of 0.3, when mitomycin C was added to 1 μg/ml to one-half of the culture, and growth was allowed to proceed for one additional hour. Cells were chloroform permeabilized and assayed for β-galactosidase as described by Miller (72). Activity values are the averages of several independent determinations.