ArticlePloS one2017
The PAPI-1 pathogenicity island-encoded small RNA PesA influences Pseudomonas aeruginosa virulence and modulates pyocin S3 production.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Small regulatory RNAs mediated regulation of virulence and host-pathogen interaction in the Gram-negative ESKAPE pathogens.Virulence · 2026Review
- MOBHunter: a data integration platform for identification and classification of mobile genetic elements in microbial genomes.Nucleic acids research · 2025Article
- The function of small RNA inPeerJ · 2022Article
- The horizontal transfer of Pseudomonas aeruginosa PA14 ICE PAPI-1 is controlled by a transcriptional triad between TprA, NdpA2 and MvaT.Nucleic acids research · 2021Article
- Diversity and Versatility in Small RNA-Mediated Regulation in Bacterial Pathogens.Frontiers in microbiology · 2021Review
- The Small RNA ErsA Impacts the Anaerobic Metabolism ofFrontiers in microbiology · 2021Article
- The Small RNA ErsA Plays a Role in the Regulatory Network of Pseudomonas aeruginosa Pathogenicity in Airway Infections.mSphere · 2020Article
- AtxA-Controlled Small RNAs ofFrontiers in microbiology · 2020Article
- Small Noncoding Regulatory RNAs fromInternational journal of molecular sciences · 2018Review
- Negative Control of RpoS Synthesis by the sRNA ReaL inFrontiers in microbiology · 2018Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small non-coding RNAs (sRNAs) are post-transcriptional regulators of gene expression that have been recognized as key contributors to bacterial virulence and pathogenic mechanisms. In this study, we characterized the sRNA PesA of the opportunistic human pathogen Pseudomonas aeruginosa. We show that PesA, which is transcribed within the pathogenicity island PAPI-1 of P. aeruginosa strain PA14, contributes to P. aeruginosa PA14 virulence. In fact, pesA gene deletion resulted in a less pathogenic strain, showing higher survival of cystic fibrosis human bronchial epithelial cells after infection. Moreover, we show that PesA influences positively the expression of pyocin S3 whose genetic locus comprises two structural genes, pyoS3A and pyoS3I, encoding the killing S3A and the immunity S3I proteins, respectively. Interestingly, the deletion of pesA gene results in increased sensitivity to UV irradiation and to the fluoroquinolone antibiotic ciprofloxacin. The degree of UV sensitivity displayed by the PA14 strain lacking PesA is comparable to that of a strain deleted for pyoS3A-I. These results suggest an involvement of pyocin S3 in DNA damage repair and a regulatory role of PesA on this function.
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