The Pyocin Regulator PrtR Regulates Virulence Expression of Pseudomonas aeruginosa by Modulation of Gac/Rsm System and c-di-GMP Signaling Pathway

Jiao, Hongying; Li, Fan; Wang, Tietao; Yam, Joey Kuok Hoong; Yang, Liang; Liang, Haihua

doi:10.1128/iai.00602-20

Cited by 12 publications

(8 citation statements)

References 54 publications

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“…In vitro, biofilm was measured according to the methods previously described with slight modifications ( 55 , 56 ). Observation of biofilm formation was carried out in 5 mL borosilicate tubes.…”

Section: Methodsmentioning

confidence: 99%

Alkaline phosphatase LapA regulates quorum sensing–mediated virulence and biofilm formation in Pseudomonas aeruginosa PAO1 under phosphate depletion stress

Tan,

Cheng,

Xiao

et al. 2023

Microbiol Spectr

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Among various environmental stresses, the depletion of inorganic phosphate, which is an important signaling molecule that modulates virulence production, is notable. In our previous study, we demonstrated that lap A, encoding alkaline phosphatase, plays a key role in Pseudomonas aeruginosa biofilm formation in porcine skin explants, an ex vivo chronic wound model. However, the mechanism by which lap A participates in the virulence and biofilm formation of P. aeruginosa remains unclear. In the present study, the lap A deletion mutant was constructed in P. aeruginosa PAO1, and the phenotypic characterization was assessed. Our data demonstrated that phosphate depletion stress significantly enhanced elastase activity, hemolysis, rhamnolipid production, swarming and swimming motilities, and 3-oxo-C12-homoserine lactone (HSL) production in P. aeruginosa . Moreover, phosphate starvation evidently induced the virulence of P. aeruginosa in Caenorhabditis elegans ( C. elegans ) through fast-kill and slow-kill infections. Deletion of the lap A gene led to broad phenotypic changes, including reduced elastase activity, swimming motility, C4-HSL, and 3-oxo-C12-HSL production, as well as increased chitinase activity and rhamnolipid production under phosphate depletion stress, which was unrelated to C4-HSL. Deletion of the lap A gene also significantly inhibited PAO1 biofilm formation in porcine skin explants by reducing the expression levels of las and rhl quorum sensing systems and extracellular polymeric substance synthesis. Finally, lap A deletion also reduced the virulence of PAO1 in C. elegans in fast-kill and slow-kill infection assays. Thus, the findings suggest that targeting lap A can help control biofilm formation and reduce virulence in nonhealing-infected wounds, where P. aeruginosa is a persistent problem. IMPORTANCE Our previous study demonstrated that the expression of lapA was induced under phosphate depletion conditions, but its roles in virulence and biofilm formation by Pseudomonas aeruginosa remain largely unknown. This study presents a systematic investigation of the roles of lapA in virulence induction and biofilm formation by constructing a lapA-deficient strain with P. aeruginosa PAO1. The results showed that deletion of the lapA gene evidently reduced elastase activity, swimming motility, C4-HSL, and 3-oxo-C12-HSL production, and increased rhamnolipid production under phosphate depletion stress. Moreover, lapA gene deletion inhibited PAO1 biofilm formation in porcine skin explants by reducing the expression levels of las and rhl quorum sensing systems and extracellular polymeric substance synthesis. Finally, lapA gene deletion also reduced the virulence of PAO1 in Caenorhabditis elegans in fast-kill and slow-kill infection assays. This study provides insights into the roles of lapA in modulating P. aeruginosa virulence and biofilm formation under phosphate depletion stress.

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Section: Methodsmentioning

confidence: 99%

Alkaline phosphatase LapA regulates quorum sensing–mediated virulence and biofilm formation in Pseudomonas aeruginosa PAO1 under phosphate depletion stress

Tan,

Cheng,

Xiao

et al. 2023

Microbiol Spectr

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“…The upstream regulatory pathway of RsmA/N is incredibly complex. RsmY/Z are regulated by many components: (1) the atypical TCS GacS/GacA in which GacS is regulated by the sensor kinases LadS (lost adherence) and RetS (regulator of exopolysaccharides and type III secretion) [177]; (2) the RNase YbeY [178]; (3) the pyocin regulator PrtR, an λCI (phage λ protein CI) homologue [179,180]; (4) the transcriptional regulator NrtR (Nudix-related transcriptional regulator) [181,182]; (5) the RNA-binding protein RtcB (RNA terminal phosphate cyclase) [183]; and (6) the transcriptional regulator from the TCS AlgZ/AlgR (alginate biosynthesis) [184]. The histidine kinase GacS is repressed by RetS via the formation of hetero-oligomers that prevent GacS phosphorylation [185].…”

Section: Posttranscriptional Regulationmentioning

confidence: 99%

Regulation of type VI secretion systems at the transcriptional, posttranscriptional and posttranslational level

Hespanhol,

Nóbrega-Silva,

Bayer-Santos

2023

Microbiology

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Bacteria live in complex polymicrobial communities and are constantly competing for resources. The type VI secretion system (T6SS) is a widespread antagonistic mechanism used by Gram-negative bacteria to gain an advantage over competitors. T6SSs translocate toxic effector proteins inside target prokaryotic cells in a contact-dependent manner. In addition, some T6SS effectors can be secreted extracellularly and contribute to the scavenging scarce metal ions. Bacteria deploy their T6SSs in different situations, categorizing these systems into offensive, defensive and exploitative. The great variety of bacterial species and environments occupied by such species reflect the complexity of regulatory signals and networks that control the expression and activation of the T6SSs. Such regulation is tightly controlled at the transcriptional, posttranscriptional and posttranslational level by abiotic (e.g. pH, iron) or biotic (e.g. quorum-sensing) cues. In this review, we provide an update on the current knowledge about the regulatory networks that modulate the expression and activity of T6SSs across several species, focusing on systems used for interbacterial competition.

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“…In colicin E7, this domain has been described as a novel alpha/beta fold containing a Zn2+ ion binding site 40 .Bacteriocin amino acid identity with that of colicinIa and is predicted to be structurally homologous to colicinsIa, B, S4 and N 42 . Pyocin S5, like the pore-forming colicins, does not form a complex with its cognate immunity protein prior to release 43 . The putative S immunity (SI) protein confers resistance to pyocin S in P. aeruginosa.…”

Section: Self-immunity Of Pyocins S Typementioning

confidence: 99%

Soluble Antimicrobial Peptide Pyocin of Pseudomonas aeruginosa and its Therapeutics: A Review Article

Sura Saleem Alberman,

EssamFadel Al-wan Al-Jumaili

2022

Indian Journal of Forensic Medicine & Toxicology

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Pyocinsis a bacteriocin produced by a group of Gram-ngative bacteria that belongs to Pseudomonasspecies. Pyocin is classified as a two distinct families of pyocins. (i) S-type pyocins (colicin-like bacteriocins), (ii) Tailocins (high-molecular weight bacteriocins that resemble phage tails).The structure of S-type pyocin is similar to that of colicin except that many S-type pyocins have three domains. Under normal conditions, the expression of prtN is repressed by PrtR. Upon exposure to stress conditions, such as DNA damage by chemicals or ultraviolet irradiation, an activated RecA triggers autoproteolytic cleavage of PrtR, which abrogates prtN repression and leads to pyocinproduction. The outer membrane receptors for three pyocins have been identified. These are FpvAI, FpvAII and FptA, all of which are involved in the uptake of iron-siderophore complexes. Before being translocated through the membrane and killing their target.This is becoming increasingly important as microbial imbalances in the natural gut flora have been suggested to play a role in a range of chronic diseases such as inflammatory bowel disease, diabetes, obesity and rheumatoid arthritis.Pyocin has now been shown to have antimicrobial activity againstbacteria in a biofilm is a limiting factor in the successful treatment of a range of chronic infections.

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The Pyocin Regulator PrtR Regulates Virulence Expression of Pseudomonas aeruginosa by Modulation of Gac/Rsm System and c-di-GMP Signaling Pathway

Cited by 12 publications

References 54 publications

Alkaline phosphatase LapA regulates quorum sensing–mediated virulence and biofilm formation in Pseudomonas aeruginosa PAO1 under phosphate depletion stress

Alkaline phosphatase LapA regulates quorum sensing–mediated virulence and biofilm formation in Pseudomonas aeruginosa PAO1 under phosphate depletion stress

Regulation of type VI secretion systems at the transcriptional, posttranscriptional and posttranslational level

Soluble Antimicrobial Peptide Pyocin of Pseudomonas aeruginosa and its Therapeutics: A Review Article

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