ArticleGut microbes2016
The synthesis of OspD3 (ShET2) in Shigella flexneri is independent of OspC1.
Article in Gut microbes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Epithelial Cell Infection Analyses with Shigella.Journal of visualized experiments : JoVE · 2024Article
- Occurrence of shigellosis in pediatric diarrheal patients in Chattogram, Bangladesh: A molecular based approach.PloS one · 2023Article
- A Versatile Human Intestinal Organoid-Derived Epithelial Monolayer Model for the Study of Enteric Pathogens.Microbiology spectrum · 2021Article
- A unique bacterial tactic to circumvent the cell death crosstalk induced by blockade of caspase-8.The EMBO journal · 2020Article
- Antibiofilm Activity of Lactobacillus plantarum 12 Exopolysaccharides against Shigella flexneri.Applied and environmental microbiology · 2020Article
- Article
- Bacteriophage Therapy Testing Against Shigella flexneri in a Novel Human Intestinal Organoid-Derived Infection Model.Journal of pediatric gastroenterology and nutrition · 2019Article
- Analysis of Shigella flexneri Resistance, Biofilm Formation, and Transcriptional Profile in Response to Bile Salts.Infection and immunity · 2017Article
- How Do the Virulence Factors ofFrontiers in cellular and infection microbiology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Shigella flexneri is a Gram-negative pathogen that invades the colonic epithelium and causes millions of cases of watery diarrhea or bacillary dysentery predominately in children under the age of 5 years in developing countries. The effector Shigella enterotoxin 2 (ShET2), or OspD3, is encoded by the sen or ospD3 gene on the virulence plasmid. Previous literature has suggested that ospD3 is in an operon downstream of the ospC1 gene, and expression of both genes is controlled by a promoter upstream of ospC1. Since the intergenic region is 328 bases in length and contains several putative promoter regions, we hypothesized the genes are independently expressed. Here we provide data that ospD3 and ospC1 are not co-transcribed and that OspC1 is not required for OspD3/ShET2 function. Most importantly, we identified strong promoter activity in the intergenic region and demonstrate that OspD3/ShET2 can be expressed and secreted independently of OspC1. This work increases our understanding of the synthesis of a unique virulence factor and provides further insights into Shigella pathogenesis.
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Registered trials
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.