TABLE 2 .
Parental strain (and evolved strain[s]) | SCV mutation | srrAB mutation | Mean fitness ± SD | Kan MIC |
---|---|---|---|---|
AH704 | menA E72K | 0.28 ± 0.01 | 64 | |
AH631 | menB G81* | 0.25 ± 0.01 | 64 | |
AH846 | menB D98G | 0.27 ± 0.02 | 48 | |
AH1560 | menB D98G | srrB T373K | 0.53 ± 0.02 | 48 |
AH841 | menB G121D | 0.29 ± 0.01 | 64 | |
AH1576 | menB G121D | srrB T373K | 0.38 ± 0.00 | 48 |
AH635 | menE Y31* | 0.28 ± 0.02 | 32 | |
AH1570 | menE Y31* | srrA M55I | 0.41 ± 0.01 | 32 |
AH839 | hemE A211fs | 0.36 ± 0.01 | 48 | |
AH1643 | hemE A211fs | srrB A250T | 0.57 ± 0.01 | 48 |
AH1647 | hemE A211fs | srrB A487T | 056 ± 0.00 | 48 |
Growth-compensatory mutations were selected by serial passage of 5 lineages of each of 6 SCV parental strains for 150 generations in LB supplemented with 15 mg/liter kanamycin. Growth compensation occurred in 7 lineages. Mutations in srrA or srrB were identified in 5 of these lineages. (Genotypes and phenotypes of the evolved strains are shown in boldface.) All growth-compensated mutants grow significantly faster than the respective parental strains (t test, P < 0.001).