Please use this identifier to cite or link to this item:
http://hdl.handle.net/10261/12019
Share/Export:
![]() ![]() |
|
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL | DATACITE | |
Title: | The Pseudomonas aeruginosa pfpI gene plays an antimutator role and provides general stress protection |
Authors: | Rodríguez-Rojas, Alexandro; Blázquez, Jesús | Keywords: | Pseudomonas aeruginosa antimutator stress |
Issue Date: | Feb-2009 | Publisher: | American Society for Microbiology | Citation: | Journal of bacteriology 191(3): 844-850 (2009) | 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 H2O2-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. | Publisher version (URL): | http://jb.asm.org/cgi/reprint/191/3/844 | URI: | http://hdl.handle.net/10261/12019 | DOI: | 10.1128/JB.01081-08 |
Appears in Collections: | (CNB) Artículos |
Files in This Item:
File | Description | Size | Format | |
---|---|---|---|---|
pfpI-Alexandro-2009.pdf | 348,43 kB | Adobe PDF | ![]() View/Open |
Review this work
PubMed Central
Citations
18
checked on May 1, 2022
SCOPUSTM
Citations
37
checked on May 14, 2022
WEB OF SCIENCETM
Citations
38
checked on May 13, 2022
Page view(s)
343
checked on May 18, 2022
Download(s)
130
checked on May 18, 2022
Google ScholarTM
Check
Altmetric
Dimensions
Related articles:
WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.