Fig. 6.

Genetic epistasis tests at the micF promoter between PC mutants of Rob’s class II surface and substitution R603A of σ⁷⁰. Plasmid pBAD33-Rob carrying the gene for wild-type Rob or PC mutant alleles of it (L74A, D75A, L78A, or Q85A) and compatible plasmid pVR-σ⁷⁰ carrying the gene for wild-type σ⁷⁰ or substitution R603A of it were introduced into strain RA4468 carrying a transcriptional fusion of lac to the micF promoter on a single-copy λ prophage. The β-galactosidase activity of the strain containing wild-type σ⁷⁰ in combination with wild-type Rob is set to 100%, and the activity produced by each mutant gene or combination of mutant genes is presented as a percentage of the wild-type activity. (a) (Left) Nonepistatic interaction between R603A and L74A. (Right) Epistatic interaction between R603A and D75A. (b) (Left) Non-epistatic interaction between R603A and L78A. (Right) Non-epistatic interaction between R603A and Q85A. (*) The p-values given in the panels denote a statistically significant difference (or no statistically significant difference) between the β-galactosidase activity produced by the single mutant that confers the most severe defect and that produced by the corresponding double mutant (both identified with an asterisk), where the activity of the double mutant is significantly less (is not significantly less) than the activity produced by either single mutant (i.e., a non-epistatic or an epistatic interaction, respectively).