Minimal inhibiting AgNO3 concentration (MICs) in the gram-negative bacteria Escherichia coli K12, Serratia proteamaculans 94, and Serratia liquefaciens MG1 were found to be on the average within the range of 0.075-0.3 microg/ml, and for Pseudomonas aeruginosa PAO1 and P. chlororaphis 449, 0.15-0.3 microg/ml. Biofilm formation in Escherichia coli AB1157 and S. Proteamaculans 94 was completely inhibited at an AgNO3 concentration of 0.3 microg/ml, and in Pseudomonas aeruginosa PAO1, at 0.6 microg/mlAgNO3. Mutations in E. coli genes encoding for global regulators of gene expression, such as sigma S and sigma N subunits of RNA polymerase, catabolite repression protein CRP, and Lon protease, had no marked effect on the sensitivity of cells to silver. The wild-type E. coli strains and strains deficient in excision repair (uvrA, uvrB), SOS-repair or recombination (recA, lexA, recBC, recF mutants) did not differ in their silver sensitivity. This suggests that the sensitivity of bacteria to silver does not correlate with DNA lesions that could be repaired by these repair and recombination systems. E. coli mutant strains deficient in porins OmpF or OmpC, were 3-4-fold more resistant to silver ions as compared with the wild-type strain. Experiments with pME6863 plasmid harboring the gene of N-acyl-homoserine lactonase AiiA demonstrated that Quorum Sensing regulation (QS) did not participate in the control of S. proteamaculans 94 and P. chlororaphis 449 silver sensitivity. The same conclusion was drawn from the comparison of AgNO3 MICs for the S. liquefaciens wild-type strain and a mutant strain deficient in QS.

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