Fig. 5.

Genetic epistasis tests at the fumC promoter between PC mutants of Rob’s class II surface and mutant alleles 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 mutant alleles of it (K593A or R599A) in all possible combinations were introduced into strain RA4468 carrying a transcriptional fusion of lac to the fumC 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) The left panel shows that K593A and R599A are not epistatic to L74A, while the right panel shows that K593A is not epistatic to D75A but R599A is epistatic to D75A. (b) The left panel shows that K593A and R599A are not epistatic to L78A, while the right panel shows that K593A and R599A are not epistatic to 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 interaction or an epistatic interaction, respectively).