Evidence map›Paper›PMID 29252102›Full record

ArticleVirulence2018

The Vibrio alginolyticus T3SS effectors, Val1686 and Val1680, induce cell rounding, apoptosis and lysis of fish epithelial cells.

Zhe Zhao, Jinxin Liu, Yiqin Deng, Wen Huang, Chunhua Ren, Douglas R Call, Chaoqun Hu

Open access · goldAbstract read
In one paragraph

Article in Virulence, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 37 citations in OpenAlex.

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  16. Virulence ofFrontiers in immunology · 2021
    Article
  17. Article
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  19. Type III Secretion 1 Effector Gene Diversity AmongFrontiers in cellular and infection microbiology · 2020
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Zhe Zhaoa Institute of Marine Biology, College of Oceanography, Hohai University , Nanjing , Jiangsu, PR China.
Jinxin Liua Institute of Marine Biology, College of Oceanography, Hohai University , Nanjing , Jiangsu, PR China.
Yiqin Dengb Key Laboratory of Marine Bio-resources Sustainable Utilization, Key Laboratory of Applied Marine Biology of Guangdong Province, South China Sea Institute of Oceanology, Chinese Academy of Sciences , Guangzhou, Guangdong , PR China.
Wen Huangb Key Laboratory of Marine Bio-resources Sustainable Utilization, Key Laboratory of Applied Marine Biology of Guangdong Province, South China Sea Institute of Oceanology, Chinese Academy of Sciences , Guangzhou, Guangdong , PR China.
Chunhua Renb Key Laboratory of Marine Bio-resources Sustainable Utilization, Key Laboratory of Applied Marine Biology of Guangdong Province, South China Sea Institute of Oceanology, Chinese Academy of Sciences , Guangzhou, Guangdong , PR China.
Douglas R Callc Paul G. Allen School for Global Animal Health, Washington State University , Pullman , WA , U.S.
Chaoqun Hub Key Laboratory of Marine Bio-resources Sustainable Utilization, Key Laboratory of Applied Marine Biology of Guangdong Province, South China Sea Institute of Oceanology, Chinese Academy of Sciences , Guangzhou, Guangdong , PR China.
South China Sea Institute Of Oceanology · CNChinese Academy of Sciences · CNWashington State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vibrio alginolyticus is a Gram-negative bacterium that is an opportunistic pathogen of both marine animals and people. Its pathogenesis likely involves type III secretion system (T3SS) mediated induction of rapid apoptosis, cell rounding and osmotic lysis of infected eukaryotic cells. Herein, we report that effector proteins, Val1686 and Val1680 from V. alginolyticus, were responsible for T3SS-mediated death of fish cells. Val1686 is a Fic-domain containing protein that not only contributed to cell rounding by inhibiting Rho guanosine triphosphatases (GTPases), but was requisite for the induction of apoptosis because the deletion mutant (Δval1686) was severely weakened in its ability to induce cell rounding and apoptosis in fish cells. In addition, Val1686 alone was sufficient to induce cell rounding and apoptosis as evidenced by the transfection of Val1686 into fish cells. Importantly, the Fic-domain essential for cell rounding activity was equally important to activation of apoptosis of fish cells, indicating that apoptosis is a downstream event of Val1686-dependent GTPase inhibition. V. alginolyticus infection likely activates JNK and ERK pathways with sequential activation of caspases (caspase-8/-10, -9 and -3) and subsequent apoptosis. Val1680 contributed to T3SS-dependent lysis of fish cells in V. alginolyticus, but did not induce autophagy as has been reported for its homologue (VopQ) in V. parahaemolyticus. Together, Val1686 and Val1680 work together to induce apoptosis, cell rounding and cell lysis of V. alginolyticus-infected fish cells. These findings provide new insights into the mechanism of cell death caused by T3SS of V. alginolyticus.

Indexed as

ApoptosisAnimalsCells, CulturedCell ShapeCytotoxinsEpithelial CellsFishesGene DeletionType III Secretion SystemsVibrio alginolyticusVirulence FactorsCytotoxinsType III Secretion SystemsVirulence Factorsapoptosiseffector proteinfish diseaseT3SSVibrio alginolyticus

Identifiers

PMID29252102
PMCPMC5955196
OpenAlexW2777667033

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.