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. Author manuscript; available in PMC: 2015 May 1.
Published in final edited form as: Mol Microbiol. 2014 Apr 9;92(3):488–506. doi: 10.1111/mmi.12587

Figure 7. Modulation of c-di-GMP levels, but not aggregative behavior, contributes to P. aeruginosa resistance to antimicrobial agents.

Figure 7

(A) Images demonstrate growth and aggregation of P. aeruginosa PAO1, PAO1/pJN-PA4843, Δpsl/pJN-PA4843, and PAO1/pJN-PA4843/pMJT-dipA in liquid and demonstrate that the hyperaggregative phenotype of PAO1/pJN-PA4843 depends on the presence of the Psl polysaccharide and elevated levels of c-di-GMP. (B) Overexpression of PA4843 does not affect growth in liquid. Due to differences in the aggregative phenotypes of the strains, bacterial cultures were homogenized prior to determining the turbidity at 600 nm. (C–D) Multicopy expression of PA4843 in P. aeruginosa PAO1 and Δpsl mutant renders P. aeruginosa more resistant to (C) tobramycin (50 μg/ml) and (D) norfloxacin (150 μg/ml). All planktonic cells were treated for 1 hr and experiments were done in triplicate. Error bars denote standard deviation. *, Significantly different from PAO1, p < 0.01 as determined by ANOVA and SigmaStat.