Temperature-specific expression of cspA1 contributes to activation of sigX during pathogenesis and intracellular survival in Pseudomonas plecoglossicida

Huang, Lixing; Zhao, Lingmin; Qi, Weilu; Xu, Xiaojin; Zhang, Jiaonan; Zhang, Jiao‐Lin; Yan, Qingpi

doi:10.1016/j.aquaculture.2019.734861

Cited by 17 publications

(8 citation statements)

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“…Another major finding of this study is the increased sigX expression following an alteration of the membrane properties or CS. In addition, these results are in agreement with a recent publication, which shows that CspA1 contributes to SigX expression in Pseudomonas plecoglossicida (Huang et al, 2020). This result also reinforces the hypothesis of an atypical dependent regulatory mechanism requiring further characterization.…”

Section: Discussionsupporting

confidence: 92%

The Temperature-Regulation of Pseudomonas aeruginosa cmaX-cfrX-cmpX Operon Reveals an Intriguing Molecular Network Involving the Sigma Factors AlgU and SigX

et al. 2020

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Thermo-Regulation of the cmaX-cfrX-cmpX Operon IMPORTANCE Because temperature is one of the first physical signal that allows bacteria to distinguish a potential host from its environment, the response of P. aeruginosa has been more investigated in case of elevated rather than low temperature. Here, we show that the ECFσ SigX is an effector in the latter condition, which controls the transcription of the two members of an intriguing operon encoding the mechanosensitive channel CmpX and the hypothetical protein CfrX, while cmaX is under the control of AlgU. In addition, we show that SigX is activated following membrane structure alterations. More generally, we have identified temperature as a key environmental factor regulating antagonistically the expression and the activity of the two major cell wall stress response ECFσ in P. aeruginosa, suggesting that they are involved in specific but interconnected networks, in which the AlgU-dependent global transcriptional regulator AmrZ (alginate and motility regulator Z) could play a role by a mechanism that remains to be explored.

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Section: Discussionsupporting

confidence: 92%

The Temperature-Regulation of Pseudomonas aeruginosa cmaX-cfrX-cmpX Operon Reveals an Intriguing Molecular Network Involving the Sigma Factors AlgU and SigX

et al. 2020

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“…Pseudomonas plecoglossicida is the causative agent of "visceral white spot disease" in Epinephelus coioides and Larimichthys crocea under the water temperatures of 15-20 • C and has resulted in high mortality and heavy economic loss (Zhang et al, 2018;Huang et al, 2020). To alleviate the harm caused by P. plecoglossicida, its pathogenic mechanism has attracted much attention.…”

Section: Introductionmentioning

confidence: 99%

The Effect of tonB Gene on the Virulence of Pseudomonas plecoglossicida and the Immune Response of Epinephelus coioides

Zhao

Zhuang

et al. 2021

Front. Microbiol.

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Pseudomonas plecoglossicida is the causative agent of “visceral white spot disease” in cultured fish and has resulted in serious economic losses. tonB gene plays a crucial role in the uptake of nutrients from the outer membranes in Gram-negative bacteria. The previous results of our lab showed that the expression of tonB gene of P. plecoglossicida was significantly upregulated in the spleens of infected Epinephelus coioides. To explore the effect of tonB gene on the virulence of P. plecoglossicida and the immune response of E. coioides, tonB gene of P. plecoglossicida was knocked down by RNAi; and the differences between the wild-type strain and the tonB-RNAi strain of P. plecoglossicida were investigated. The results showed that all of the four mutants of P. plecoglossicida exhibited significant decreases in mRNA of tonB gene, and the best knockdown efficiency was 94.0%; the survival rate of E. coioides infected with the tonB-RNAi strain was 20% higher than of the counterpart infected with the wild strain of P. plecoglossicida. Meanwhile, the E. coioides infected with the tonB-RNAi strain of P. plecoglossicida carried less pathogens in the spleen and less white spots on the surface of the spleen; compared with the wild-type strain, the motility, chemotaxis, adhesion, and biofilm formation of the tonB-RNAi strain were significantly attenuated; the transcriptome data of E. coioides infected with the tonB-RNAi strain were different from the counterpart infected with the wild strain of P. plecoglossicida; the antigen processing and presentation pathway and the complement and coagulation cascade pathway were the most enriched immune pathways. The results indicated that tonB was a virulence gene of P. plecoglossicida; tonB gene was involved in the regulation of motility, chemotaxis, adhesion, and biofilm formation; tonB gene affected the immune response of E. coioides to P. plecoglossicida infection.

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“…Bacterial virulence is usually affected by environmental factors. For example, the pathogenic temperature of “visceral white spot disease” caused by P. plecoglossicida in large yellow croaker and other commercial fish is 15°C–20°C ( Zhang et al., 2018a ; Kaur et al., 2019 ; Lv et al., 2019 ; Huang et al., 2020a ; Hu et al., 2021 ; Jin et al., 2021 ). The results of various stress experiments showed that compared with 18°C, the expression level of fusA was significantly downregulated at 4°C, 12°C, and 37°C.…”

Section: Discussionmentioning

confidence: 99%

Effect of Ferredoxin Receptor FusA on the Virulence Mechanism of Pseudomonas plecoglossicida

Wang

Lin

et al. 2022

Front. Cell. Infect. Microbiol.

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Pseudomonas plecoglossicida is an aerobic Gram-negative bacterium, which is the pathogen of “Visceral white spot disease” in large yellow croaker. P. plecoglossicida is a temperature-dependent bacterial pathogen in fish, which not only reduces the yield of large yellow croaker but also causes continuous transmission of the disease, seriously endangering the healthy development of fisheries. In this study, a mutant strain of fusA was constructed using homologous recombination technology. The results showed that knockout of P. plecoglossicida fusA significantly affected the ability of growth, adhesion, and biofilm formation. Temperature, pH, H2O2, heavy metals, and the iron-chelating agent were used to treat the wild type of P. plecoglossicida; the results showed that the expression of fusA was significantly reduced at 4°C, 12°C, and 37°C. The expression of fusA was significantly increased at pH 4 and 5. Cu2+ has a significant inducing effect on the expression of fusA, but Pb2+ has no obvious effect; the expression of fusA was significantly upregulated under different concentrations of H2O2. The expression of the fusA gene was significantly upregulated in the 0.5~4-μmol/l iron-chelating agent. The expression level of the fusA gene was significantly upregulated after the logarithmic phase. It was suggested that fusA included in the TBDR family not only was involved in the transport of ferredoxin but also played important roles in the pathogenicity and environment adaptation of P. plecoglossicida.

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Temperature-specific expression of cspA1 contributes to activation of sigX during pathogenesis and intracellular survival in Pseudomonas plecoglossicida

Cited by 17 publications

References 40 publications

The Temperature-Regulation of Pseudomonas aeruginosa cmaX-cfrX-cmpX Operon Reveals an Intriguing Molecular Network Involving the Sigma Factors AlgU and SigX

The Temperature-Regulation of Pseudomonas aeruginosa cmaX-cfrX-cmpX Operon Reveals an Intriguing Molecular Network Involving the Sigma Factors AlgU and SigX

The Effect of tonB Gene on the Virulence of Pseudomonas plecoglossicida and the Immune Response of Epinephelus coioides

Effect of Ferredoxin Receptor FusA on the Virulence Mechanism of Pseudomonas plecoglossicida

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