scholarly journals Corrigendum: Transcriptional Regulation of the Type VI Secretion System 1 Genes by Quorum Sensing and ToxR in Vibrio parahaemolyticus

2020 ◽  
Vol 11 ◽  
Author(s):  
Yiquan Zhang ◽  
He Gao ◽  
George Osei-Adjei ◽  
Ying Zhang ◽  
Wenhui Yang ◽  
...  
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.


Microbiology ◽  
2014 ◽  
Vol 160 (9) ◽  
pp. 1867-1873 ◽  
Author(s):  
Dor Salomon ◽  
John A. Klimko ◽  
Kim Orth

The marine bacterium Vibrio parahaemolyticus, a major cause of food-borne gastroenteritis, employs a type VI secretion system 1 (T6SS1), a recently discovered protein secretion system, to combat competing bacteria. Environmental signals such as temperature, salinity, cell density and surface sensing, as well as the quorum-sensing master regulator OpaR, were previously reported to regulate T6SS1 activity and expression. In this work, we set out to identify additional transcription regulators that control the tightly regulated T6SS1 activity. To this end, we determined the effect of deletions in several known virulence regulators and in two regulators encoded within the T6SS1 gene cluster on expression and secretion of the core T6SS component Hcp1 and on T6SS1-mediated anti-bacterial activity. We report that VP1391 and VP1407, transcriptional regulators encoded within the T6SS1 gene cluster, are essential for T6SS1 activity. Moreover, we found that H-NS, a bacterial histone-like nucleoid structuring protein, which mediates transcription silencing of horizontally acquired genes, serves as a repressor of T6SS1. We also show that activation of surface sensing and high salt conditions alleviate the H-NS-mediated repression. Our results shed light on the complex network of environmental signals and transcription regulators that govern the tight regulation over T6SS1 activity.


PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e73363 ◽  
Author(s):  
Li Wang ◽  
Dongsheng Zhou ◽  
Panyong Mao ◽  
Yiquan Zhang ◽  
Jun Hou ◽  
...  

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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