CqsA-introduced quorum sensing inhibits type VI secretion system 2 through an OpaR-dependent pathway in Vibrio parahaemolyticus

2021 ◽  
pp. 105334
Author(s):  
Kui Wu ◽  
Yongyan Long ◽  
Qian Liu ◽  
Wei Wang ◽  
Guoyin Fan ◽  
...  
PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e73363 ◽  
Author(s):  
Li Wang ◽  
Dongsheng Zhou ◽  
Panyong Mao ◽  
Yiquan Zhang ◽  
Jun Hou ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Lizhi Ma ◽  
Yiquan Zhang ◽  
Xiaojuan Yan ◽  
Liping Guo ◽  
Li Wang ◽  
...  

The type VI secretion system (T6SS) is bacterial protein injection machinery with roles in virulence, symbiosis, interbacterial interaction, antipathogenesis, and environmental stress responses. There are two T6SS loci, T6SS1 and T6SS2, in the two chromosomes ofVibrio parahaemolyticus, respectively. This work disclosed that the master quorum sensing (QS) regulator OpaR repressed the transcription ofhcp1encoding the structural component Hcp1 of T6SS1 inV. parahaemolyticus, indicating that QS had a negative regulatory action on T6SS1. A singleσ54-dependent promoter was transcribed forhcp1inV. parahaemolyticus, and its activity was repressed by the OpaR regulator. Since the OpaR protein could not bind to the upstream region ofhcp1, OpaR would repress the transcription ofhcp1in an indirect manner.


2020 ◽  
Vol 149 ◽  
pp. 104579
Author(s):  
Yue Qiu ◽  
Lingfei Hu ◽  
Wenhui Yang ◽  
Zhe Yin ◽  
Dongsheng Zhou ◽  
...  

2017 ◽  
Vol 83 (13) ◽  
Author(s):  
Peng Li ◽  
Lisa N. Kinch ◽  
Ann Ray ◽  
Ankur B. Dalia ◽  
Qian Cong ◽  
...  

ABSTRACT Acute hepatopancreatic necrosis disease (AHPND) is a newly emerging shrimp disease that has severely damaged the global shrimp industry. AHPND is caused by toxic strains of Vibrio parahaemolyticus that have acquired a “selfish plasmid” encoding the deadly binary toxins PirAvp/PirBvp. To better understand the repertoire of virulence factors in AHPND-causing V. parahaemolyticus, we conducted a comparative analysis using the genome sequences of the clinical strain RIMD2210633 and of environmental non-AHPND and toxic AHPND isolates of V. parahaemolyticus. Interestingly, we found that all of the AHPND strains, but none of the non-AHPND strains, harbor the antibacterial type VI secretion system 1 (T6SS1), which we previously identified and characterized in the clinical isolate RIMD2210633. This finding suggests that the acquisition of this T6SS might confer to AHPND-causing V. parahaemolyticus a fitness advantage over competing bacteria and facilitate shrimp infection. Additionally, we found highly dynamic effector loci in the T6SS1 of AHPND-causing strains, leading to diverse effector repertoires. Our discovery provides novel insights into AHPND-causing pathogens and reveals a potential target for disease control. IMPORTANCE Acute hepatopancreatic necrosis disease (AHPND) is a serious disease that has caused severe damage and significant financial losses to the global shrimp industry. To better understand and prevent this shrimp disease, it is essential to thoroughly characterize its causative agent, Vibrio parahaemolyticus. Although the plasmid-encoded binary toxins PirAvp/PirBvp have been shown to be the primary cause of AHPND, it remains unknown whether other virulent factors are commonly present in V. parahaemolyticus and might play important roles during shrimp infection. Here, we analyzed the genome sequences of clinical, non-AHPND, and AHPND strains to characterize their repertoires of key virulence determinants. Our studies reveal that an antibacterial type VI secretion system is associated with the AHPND strains and differentiates them from non-AHPND strains, similar to what was seen with the PirA/PirB toxins. We propose that T6SS1 provides a selective advantage during shrimp infections.


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