Fig. 2.

Cheater resistance is lost by removing endogenous plasmid pBS32 or the rapP gene on it. a ∆srfAA cheating assays as in Fig. 1, with strains of NCIB 3610 either missing the plasmid (∆pBS32) or with the rapP gene interrupted by a transposon insertion (∆rapP). Total cell yield of each swarm normalized to the value of wild-type alone (0% mutant); averages of four (0% and 100%) or two replicates (all others). Relative fitness of the ∆srfAA mutant; each point is the mean ± SEM of independent biological replicates (0% n = 4, others n = 2). All yields were significantly different from wild-type alone (P < 0.0001) except ∆rapP 10% and 90% (P = 0.0388 and 0.0950); for fitness measurements, 10% and 33% mutant were statistically significant in both ∆pBS32 (P < 0.0001 and 0.0009) and ∆rapP (P = 0.0019 and 0.0477). b Cheating assays in which rapPphrP or rapP(T236N)phrP has been inserted into the chromosome of PS-216 or NCIB 3610 ∆pBS32. Statistically significant swarm yields included PS-216 + rapP 90% and 100% (P = 0.0003 and <0.0001), ∆pBS32 + rapP 67%, 90%, and 100% (P = 0.0102, <0.0001, <0.0001), and all ∆pBS32 + rapP(T236N) values (10% P = 0.0006, others P < 0.0001). Neither rapP addback had significant fitness values, but all ∆pBS32 + rapP(T236N) were significant (P < 0.0001 for all but 90% P = 0.0004)