Evidence map›Paper›PMID 26341202›Full record

ArticleApplied and environmental microbiology2015

Positive Regulation of Staphylococcal Enterotoxin H by Rot (Repressor of Toxin) Protein and Its Importance in Clonal Complex 81 Subtype 1 Lineage-Related Food Poisoning.

Yusuke Sato'o, Junzo Hisatsune, Yuria Nagasako, Hisaya K Ono, Katsuhiko Omoe, Motoyuki Sugai

Open access · bronzeAbstract read
In one paragraph

Article in Applied and environmental microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-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

11 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Yusuke Sato'oDepartment of Bacteriology, Hiroshima University Graduate School of Biomedical & Health Sciences, Hiroshima City, Hiroshima, Japan The United Graduate School of Veterinary Sciences, Gifu University, Gifu City, Gifu, Japan Department of Veterinary Medicine, Faculty of Agriculture, Iwate University, Morioka, Iwate, Japan.
Junzo HisatsuneDepartment of Bacteriology, Hiroshima University Graduate School of Biomedical & Health Sciences, Hiroshima City, Hiroshima, Japan.
Yuria NagasakoDepartment of Veterinary Medicine, Faculty of Agriculture, Iwate University, Morioka, Iwate, Japan.
Hisaya K OnoDepartment of Microbiology and Immunology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Katsuhiko OmoeThe United Graduate School of Veterinary Sciences, Gifu University, Gifu City, Gifu, Japan Department of Veterinary Medicine, Faculty of Agriculture, Iwate University, Morioka, Iwate, Japan.
Motoyuki SugaiDepartment of Bacteriology, Hiroshima University Graduate School of Biomedical & Health Sciences, Hiroshima City, Hiroshima, Japan sugai@hiroshima-u.ac.jp.
Hiroshima University · JPGifu University · JPHirosaki University · JPIwate University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously demonstrated the clonal complex 81 (CC81) subtype 1 lineage is the major staphylococcal food poisoning (SFP)-associated lineage in Japan (Y. Sato'o et al., J Clin Microbiol 52:2637-2640, 2014, http://dx.doi.org/10.1128/JCM.00661-14). Strains of this lineage produce staphylococcal enterotoxin H (SEH) in addition to SEA. However, an evaluation of the risk for the recently reported SEH has not been sufficiently conducted. We first searched for staphylococcal enterotoxin (SE) genes and SE proteins in milk samples that caused a large SFP outbreak in Japan. Only SEA and SEH were detected, while there were several SE genes detected in the samples. We next designed an experimental model using a meat product to assess the productivity of SEs and found that only SEA and SEH were detectably produced in situ. Therefore, we investigated the regulation of SEH production using a CC81 subtype 1 isolate. Through mutant analysis of global regulators, we found the repressor of toxin (Rot) functioned oppositely as a stimulator of SEH production. SEA production was not affected by Rot. seh mRNA expression correlated with rot both in media and on the meat product, and the Rot protein was shown to directly bind to the seh promoter. The seh promoter sequence was predicted to form a loop structure and to hide the RNA polymerase binding sequences. We propose Rot binds to the promoter sequence of seh and unfolds the secondary structure that may lead the RNA polymerase to bind the promoter, and then seh mRNA transcription begins. This alternative Rot regulation for SEH may contribute to sufficient toxin production by the CC81 subtype 1 lineage in foods to induce SFP.

Indexed as

Gene Expression Regulation, BacterialAnimalsBacterial ProteinsEnterotoxinsJapanMilkMultiplex Polymerase Chain ReactionReal-Time Polymerase Chain ReactionRepressor ProteinsStaphylococcal Food PoisoningStaphylococcus aureusBacterial ProteinsEnterotoxinsRepressor Proteinsrot protein, Staphylococcus aureusStaphylococcal enterotoxin H

Identifiers

PMID26341202
PMCPMC4616944
OpenAlexW2228998419

What OpenQuestion holds

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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 OpenQuestion graph.