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PMID:19028889
| Citation |
Rodríguez-Rojas, A and Blázquez, J (2009) The Pseudomonas aeruginosa pfpI gene plays an antimutator role and provides general stress protection. J. Bacteriol. 191:844-50 |
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| Abstract |
Hypermutator Pseudomonas aeruginosa strains, characterized by an increased spontaneous-mutation rate, are found at high frequencies in chronic lung infections. Hypermutability is associated with the loss of antimutator genes related to DNA repair or damage avoidance systems. Only a few antimutator genes have been described in P. aeruginosa, although there is some evidence that additional genes may be involved in naturally occurring hypermutability. In order to find new P. aeruginosa antimutator genes, we constructed and screened a library of random insertions in the PA14 strain. Some previously described P. aeruginosa and/or Escherichia coli antimutator genes, such as mutS, mutL, uvrD, mutT, ung, and mutY, were detected, indicating a good coverage of our insertional library. One additional mutant contained an insertion in the P. aeruginosa PA14-04650 (pfpI) gene, putatively encoding a member of the DJ-1/ThiJ/PfpI superfamily, which includes chaperones, peptidases, and the Parkinson's disease protein DJ-1a. The pfpI-defective mutants in both PAO1 and PA14 showed higher spontaneous mutation rates than the wild-type strains, suggesting that PfpI plays a key role in DNA protection under nonstress conditions. Moreover, the inactivation of pfpI resulted in a dramatic increase in the H(2)O(2)-induced mutant frequency. Global transcription studies showed the induction of bacteriophage Pf1 genes and the repression of genes related to iron metabolism, suggesting that the increased spontaneous-mutant frequency may be due to reduced protection against the basal level of reactive oxygen species. Finally, pfpI mutants are more sensitive to different types of stress and are affected in biofilm formation. |
| Links |
PubMed PMC2632063 Online version:10.1128/JB.01081-08 |
| Keywords |
Bacterial Proteins/genetics; Bacterial Proteins/metabolism; Bacterial Proteins/physiology; Biofilms/growth & development; Hydrogen Peroxide/pharmacology; Microbial Viability/drug effects; Microbial Viability/genetics; Mutagenesis, Insertional; Mutation/drug effects; Oligonucleotide Array Sequence Analysis; Pseudomonas aeruginosa/genetics; Pseudomonas aeruginosa/metabolism; Pseudomonas aeruginosa/physiology |
| edit table |
Significance
Annotations
| Gene product | Qualifier | GO Term | Evidence Code | with/from | Aspect | Extension | Notes | Status |
|---|---|---|---|---|---|---|---|---|
| GO:0042710: biofilm formation |
ECO:0000315: |
P |
In P. aeruginosa PA14 strain, the pfpl gene when interrupted, has been shown to cause an increase in the spontaneous mutation rate. Although, when the pfpl gene is interrupted, it can also cause a deficiency in biofilm formation. Referring to Figure 4, the wild type strain and mutated strain’s biofilm formation was measured in arbitrary units. The white bars are the mutated strains, and clearly show a decrease in biofilm formation compared to the wild type. This difference between the wild type and mutated strain formation held up even after 24 hours from incubation. They obtained these measurements (a.u.) by dividing the absorbance at 595 nm after crystal violet staining by the optical density of the cells prior to staining. |
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