Expression of the AHPND Toxins PirA vp and PirB vp Is Regulated by Components of the Vibrio parahaemolyticus Quorum Sensing (QS) System

Acute hepatopancreatic necrosis disease (AHPND) in shrimp is caused by strains that harbor a pVA1-like plasmid containing the and genes. It is also known that the production of the PirA and PirB proteins, which are the key factors that drive the observed symptoms of AHPND, can be influenced by envir...

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Bibliographic Details
Published in:International journal of molecular sciences 2022-03, Vol.23 (5)
Main Authors: Lin, Shin-Jen, Huang, Jiun-Yan, Le, Phuoc-Thien, Lee, Chung-Te, Chang, Che-Chang, Yang, Yi-Yuan, Su, Emily Chia-Yu, Lo, Chu-Fang, Wang, Hao-Ching
Format: Article
Language:English
Subjects:
Animals
Necrosis
Penaeidae - microbiology
Quorum Sensing - genetics
Toxins, Biological - metabolism
Vibrio parahaemolyticus
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Summary:Acute hepatopancreatic necrosis disease (AHPND) in shrimp is caused by strains that harbor a pVA1-like plasmid containing the and genes. It is also known that the production of the PirA and PirB proteins, which are the key factors that drive the observed symptoms of AHPND, can be influenced by environmental conditions and that this leads to changes in the virulence of the bacteria. However, to our knowledge, the mechanisms involved in regulating the expression of the / genes have not previously been investigated. In this study, we show that in the AHPND-causing 3HP strain, the and genes are highly expressed in the early log phase of the growth curve. Subsequently, the expression of the PirA and PirB proteins continues throughout the log phase. When we compared mutant strains with a deletion or substitution in two of the quorum sensing (QS) master regulators, and/or ( , Δ , Δ and Δ Δ ), our results suggested that expression of the and genes was related to the QS system, with acting as a negative regulator of and without any mediation by . In the promoter region of the / operon, we also identified a putative consensus binding site for the QS transcriptional regulator AphB. Real-time PCR further showed that was negatively controlled by LuxO , and that its expression paralleled the expression patterns of and . An electrophoretic mobility shift assay (EMSA) showed that AphB could bind to this predicted region, even though another QS transcriptional regulator, AphA , could not. Taken together, these findings suggest that the QS system may regulate expression through AphB .
ISSN:1422-0067