Transcriptional regulation of the virulence genes and the biofilm formation associated operons in Vibrio parahaemolyticus

Zhang, Yiquan; Qiu, Yue; Xue, Xingfan; Zhang, Miaomiao; Sun, Junfang; Li, Xue; Hu, Lingfei; Yin, Zhe; Yang, Wenhui; Lu, Renfei; Zhou, Dongsheng

doi:10.1186/s13099-021-00410-y

Cited by 17 publications

(14 citation statements)

References 24 publications

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“…In the present work, the results of qRT-PCR displayed that most T3SS1-related genes were downregulated in Δ vmeL compared with wild type strains. A similar study found that RND null mutants increased leuO transcription in V. cholera ( Bina et al, 2018 ), and the leuO -homologous protein CalR repressed the transcription of T3SS1 in V. parahaemolyticus ( Gode-Potratz et al, 2010 ; Zhang et al, 2021b ). Therefore, we inferred that VmeL mediates cytotoxicity by indirectly modulating the transcription of T3SS1 by an unknown mechanism.…”

Section: Discussionmentioning

confidence: 72%

Biological and transcriptional studies reveal VmeL is involved in motility, biofilm formation and virulence in Vibrio parahaemolyticus

Liu

Zhang²,

Wang³

et al. 2022

Front. Microbiol.

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Vibrio parahaemolyticus is a marine pathogen thought to be the leading cause of seafood-borne gastroenteritis globally, urgently requiring efficient management methods. V. parahaemolyticus encodes 12 resistance/nodulation/division (RND) efflux systems. However, research on these systems is still in its infancy. In this study, we discovered that the inactivation of VmeL, a membrane fusion protein within the RND efflux systems, led to reduction of the ability of biofilm formation. Further results displayed that the decreased capacity of Congo red binding and the colony of ΔvmeL is more translucent compared with wild type strains, suggested reduced biofilm formation due to decreased production of biofilm exopolysaccharide upon vmeL deletion. In addition, the deletion of vmeL abolished surface swarming and swimming motility of V. parahaemolyticus. Additionally, deletion of vmeL weakened the cytotoxicity of V. parahaemolyticus towards HeLa cells, and impaired its virulence in a murine intraperitoneal infection assay. Finally, through RNA-sequencing, we ascertained that there were 716 upregulated genes and 247 downregulated genes in ΔvmeL strain. KEGG enrichment analysis revealed that quorum sensing, bacterial secretion systems, ATP-binding cassette transporters, and various amino acid metabolism pathways were altered due to the inactivation of vmeL. qRT-PCR further confirmed that genes accountable to the type III secretion system (T3SS1) and lateral flagella were negatively affected by vmeL deletion. Taken together, our results suggest that VmeL plays an important role in pathogenicity, making it a good target for managing infection with V. parahaemolyticus.

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Section: Discussionmentioning

confidence: 72%

Biological and transcriptional studies reveal VmeL is involved in motility, biofilm formation and virulence in Vibrio parahaemolyticus

Liu

Zhang²,

Wang³

et al. 2022

Front. Microbiol.

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“…Our data showed that cpsQ and mfpABC were significantly induced and repressed in the wrinkly phenotype, respectively (Table S3). Considering that QsvR and AphA activate and repress the transcription of cpsQ-mfpABC and mfpABC , respectively ( 77 , 78 ), and both were induced in the wrinkly phenotype (Table S3), genes encoding Mfp proteins should be strictly regulated and balance changes in colony morphology.…”

Section: Resultsmentioning

confidence: 99%

Transcriptomic Analysis of Vibrio parahaemolyticus Underlying the Wrinkly and Smooth Phenotypes

Zhang

et al. 2022

Microbiol Spectr

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We showed that Vibrio parahaemolyticus was able to naturally and reversibly switch between wrinkly and smooth phenotypes and disclosed the gene expression profiles related to wrinkly-smooth switching, showing that the significantly differentially expressed genes between the two colony morphology phenotypes were involved in various biological behaviors, including virulence factor production, biofilm formation, metabolism, adaptation, and colonization.

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“…This cyclic di-GMP is programmed by a capsular polysaccharide (CpsQ), which is part of the membrane fusion protein (MFP). The proteinencoding MFP locus is required for biofilm production in Vp (Zhang et al, 2021).…”

Section: Role Of Biofilm and Quorum Sensing Regulators For Adaptationsmentioning

confidence: 99%

Adaptations of Vibrio parahaemolyticus to Stress During Environmental Survival, Host Colonization, and Infection

2021

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Vibrio parahaemolyticus (Vp) is an aquatic Gram-negative bacterium that may infect humans and cause gastroenteritis and wound infections. The first pandemic of Vp associated infection was caused by the serovar O3:K6 and epidemics caused by the other serovars are increasingly reported. The two major virulence factors, thermostable direct hemolysin (TDH) and/or TDH-related hemolysin (TRH), are associated with hemolysis and cytotoxicity. Vp strains lacking tdh and/or trh are avirulent and able to colonize in the human gut and cause infection using other unknown factors. This pathogen is well adapted to survive in the environment and human host using several genetic mechanisms. The presence of prophages in Vp contributes to the emergence of pathogenic strains from the marine environment. Vp has two putative type-III and type-VI secretion systems (T3SS and T6SS, respectively) located on both the chromosomes. T3SS play a crucial role during the infection process by causing cytotoxicity and enterotoxicity. T6SS contribute to adhesion, virulence associated with interbacterial competition in the gut milieu. Due to differential expression, type III secretion system 2 (encoded on chromosome-2, T3SS2) and other genes are activated and transcribed by interaction with bile salts within the host. Chromosome-1 encoded T6SS1 has been predominantly identified in clinical isolates. Acquisition of genomic islands by horizontal gene transfer provides enhanced tolerance of Vp toward several antibiotics and heavy metals. Vp consists of evolutionarily conserved targets of GTPases and kinases. Expression of these genes is responsible for the survival of Vp in the host and biochemical changes during its survival. Advanced genomic analysis has revealed that various genes are encoded in Vp pathogenicity island that control and expression of virulence in the host. In the environment, the biofilm gene expression has been positively correlated to tolerance toward aerobic, anaerobic, and micro-aerobic conditions. The genetic similarity analysis of toxin/antitoxin systems of Escherichia coli with VP genome has shown a function that could induce a viable non-culturable state by preventing cell division. A better interpretation of the Vp virulence and other mechanisms that support its environmental fitness are important for diagnosis, treatment, prevention and spread of infections. This review identifies some of the common regulatory pathways of Vp in response to different stresses that influence its survival, gut colonization and virulence.

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Transcriptional regulation of the virulence genes and the biofilm formation associated operons in Vibrio parahaemolyticus

Cited by 17 publications

References 24 publications

Biological and transcriptional studies reveal VmeL is involved in motility, biofilm formation and virulence in Vibrio parahaemolyticus

Biological and transcriptional studies reveal VmeL is involved in motility, biofilm formation and virulence in Vibrio parahaemolyticus

Transcriptomic Analysis of Vibrio parahaemolyticus Underlying the Wrinkly and Smooth Phenotypes

Adaptations of Vibrio parahaemolyticus to Stress During Environmental Survival, Host Colonization, and Infection

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