Table 5. Omp proteins influence rex+ host viability following T4rII infection.
| Mutation | Rex plasmid | EOPa | Cell viabilityb |
|---|---|---|---|
| −1 | – | 3.0 × 10−7 | 0 |
| −1 | + | 1.0 × 10−3 | 1.0 |
| ΔompA | + | 5.0 × 10−4 | 0.5 |
| ΔompCc | + | 0.2 | –3 |
| ΔompF | + | 2.0 × 10−5 | 1 × 10−2 |
| ΔompG | + | 6.0 × 10−4 | 0.6 |
| ΔompL | + | 1.0 × 10−3 | 1 × 10−3 |
| ΔompN | + | 2.0 × 10−4 | 0.5 |
| ΔompR | + | 0.7 | –3 |
| ΔompT | + | 5.0 × 10−4 | 0.5 |
| ΔompW | + | 1.0 × 10−5 | 1 × 10−2 |
| ΔompX | + | 1.0 × 10−5 | 1 × 10−2 |
a
Efficiency of plating showing CFU arising at 30° after infection by T4rII at an MOI of 3. Average of three trials. A 100% control of T4rII infectivity was BW25113 (rex−); BW25113 (wt) carrying [pHA1] plasmid was employed as the 100% positive control of Rex activity.
b
Rex-mediated protection of host cells from T4rII challenge. Calculated using BW25113 carrying pHA1 (rex+) plasmid as 100% viability control following T4rII challenge.
c
The deletion of ompC precludes T4 phage adsorption protecting this strain against infection. Similarly, the ompR mutation inhibits ompC expression precluding T4 phage adsorption protecting this strain against infection by T4.