Ontology highlight
ABSTRACT:
PROVIDER: PRJNA610981 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11262351_1.fastq.gz | Fastqsanger.gz | |||
| SRR11262351_2.fastq.gz | Fastqsanger.gz |
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Project description:In this study, we probed factors that could influence Shigella pathogenesis. We show that in basic pH conditions, deoxycholate-induced biofilm formation and virulence of Shigella are attenuated. We utilized RNA-sequencing to investigate pathways enriched in bacterial cells in biofilms.
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Project description:Studying the pathogenesis of human-restricted microbes is challenging, since small animal models often fail to recapitulate human physiology and suffer from infection bottlenecks that confound genetic screens. Hence, the comprehensive genetic and regulatory circuits driving the infection process of major human pathogens like Shigella flexneri remain to be defined. We combined large-scale Shigella infections of enteroids and colonoids with Transposon Directed Insertion Sequencing (TraDIS) and Bayesian statistical modelling, thereby establishing the first genome-wide map of Shigella genes required to colonize human intestinal epithelium. Our study revealed the Shigella virulence effectors essential for epithelial cell invasion across geometries and intestinal segments, identified over 100 chromosomal genes involved in the process, and uncovered a post-transcriptional mechanism whereby tRNA modification enzymes exert global control of a bacterial virulence program. Our findings provide a broadly applicable framework for combining advanced organotypic tissue culture with computational tools to map human – microbe interactions at scale.
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Project description:Studying the pathogenesis of human-restricted microbes is challenging, since small animal models often fail to recapitulate human physiology and suffer from infection bottlenecks that confound genetic screens. Hence, the comprehensive genetic and regulatory circuits driving the infection process of major human pathogens like Shigella flexneri remain to be defined. We combined large-scale Shigella infections of enteroids and colonoids with Transposon Directed Insertion Sequencing (TraDIS) and Bayesian statistical modelling, thereby establishing the first genome-wide map of Shigella genes required to colonize human intestinal epithelium. Our study revealed the Shigella virulence effectors essential for epithelial cell invasion across geometries and intestinal segments, identified over 100 chromosomal genes involved in the process, and uncovered a post-transcriptional mechanism whereby tRNA modification enzymes exert global control of a bacterial virulence program. Our findings provide a broadly applicable framework for combining advanced organotypic tissue culture with computational tools to map human – microbe interactions at scale.
2025-04-03 | GSE267395 | GEO
Project description:Studying the pathogenesis of human-restricted microbes is challenging, since small animal models often fail to recapitulate human physiology and suffer from infection bottlenecks that confound genetic screens. Hence, the comprehensive genetic and regulatory circuits driving the infection process of major human pathogens like Shigella flexneri remain to be defined. We combined large-scale Shigella infections of enteroids and colonoids with Transposon Directed Insertion Sequencing (TraDIS) and Bayesian statistical modelling, thereby establishing the first genome-wide map of Shigella genes required to colonize human intestinal epithelium. Our study revealed the Shigella virulence effectors essential for epithelial cell invasion across geometries and intestinal segments, identified over 100 chromosomal genes involved in the process, and uncovered a post-transcriptional mechanism whereby tRNA modification enzymes exert global control of a bacterial virulence program. Our findings provide a broadly applicable framework for combining advanced organotypic tissue culture with computational tools to map human – microbe interactions at scale.
2025-04-03 | GSE267394 | GEO
Project description:Studying the pathogenesis of human-restricted microbes is challenging, since small animal models often fail to recapitulate human physiology and suffer from infection bottlenecks that confound genetic screens. Hence, the comprehensive genetic and regulatory circuits driving the infection process of major human pathogens like Shigella flexneri remain to be defined. We combined large-scale Shigella infections of enteroids and colonoids with Transposon Directed Insertion Sequencing (TraDIS) and Bayesian statistical modelling, thereby establishing the first genome-wide map of Shigella genes required to colonize human intestinal epithelium. Our study revealed the Shigella virulence effectors essential for epithelial cell invasion across geometries and intestinal segments, identified over 100 chromosomal genes involved in the process, and uncovered a post-transcriptional mechanism whereby tRNA modification enzymes exert global control of a bacterial virulence program. Our findings provide a broadly applicable framework for combining advanced organotypic tissue culture with computational tools to map human – microbe interactions at scale.
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Project description:Background Compelling evidence indicates that Shigella species, the etiologic agents of bacillary dysentery, as well as enteroinvasive Escherichia coli, are derived from multiple origins of Escherichia coli and form a single pathovar. To further understand the genome diversity and virulence evolution of Shigella, comparative genomic hybridization microarray analysis was employed to compare the gene content of E. coli K-12 with those of 43 Shigella strains from all serotypes. Results For the 43 strains subjected to CGH microarray analyses, the common backbone of the Shigella genome was estimated to contain more than 1,900 open reading frames, with a mean number of 729 undetectable ORFs. The mosaic distribution of absent regions indicated that insertions and/or deletions have led to the highly diversified genomes of pathogenic strains. Conclusion These results support the hypothesis that by gain and loss of functions, Shigella species became successful human pathogens through convergent evolution from diverse genomic backgrounds. Moreover, we also found many specific differences between different lineages, providing a window into understanding bacterial speciation and taxonomic relationships. Keywords: comparative genomic hybridization
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Project description:Small regulatory RNAs (sRNAs) of Shigella dysenteriae and other pathogens are vital for the regulation of virulence-associated genes and processes. Here, we characterize RyfA1, one member of a sibling pair of sRNAs produced by S. dysenteriae. Unlike its nearly identical sibling molecule RyfA2, predicted to be encoded almost exclusively by non-pathogenic species, the presence of a gene encoding RyfA1, or a RyfA1-like molecule, is strongly correlated with virulence in a variety of enteropathogens. In S. dysenteriae, the over production of RyfA1 negatively impacts the virulence-associated process of cell-to-cell spread and the expression of ompC, a gene encoding a major outer membrane protein important for the pathogenesis of Shigella. Interestingly, the production of RyfA1 is controlled by a second sRNA, here termed RyfB1; the first incidence of one regulatory small RNA controlling another in S. dysenteriae or any Shigella species.
2017-04-17 | GSE87727 | GEO
Project description:In this study, we analyzed the expression profiles of a virulence plasmid-cured strain and wild-type strain of shigella flexneri. The results showed that the genes of glp regulon were upregulated in mutant bacteria in stationary phase cultures.
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Project description:Escherichia coli is an important human pathogen, among others a cause of severe diarrhea diseases and urinary tract infections. The ability to distinguish different pathogenic E. coli subspecies is crucial for correct treatment of the infection. Characterization and quantification of clinical isolates proteomes can provide details of the organisms’ metabolism and specific virulence factors. We performed a systematic quantitative proteomic analysis on a representative selection of 16 pathogenic and 2 commensal E. coli strains, together with 5 pathogenic Shigella strains. The analysis yielded a dataset of more than 4 thousand proteins, with an average of 2 thousand proteins per strain and 980 proteins common to all strains. Statistical comparison of label-free quantitative levels of 750 proteins, which were quantified in all strains, revealed that levels of a majority of the shared proteins vary substantially among specific strains. Theses quantitative protein profiles clearly distinguished E. coli strains from Shigella and largely separated commensal E. coli strains from intestinal and extraintestinal E. coli isolates.
2020-10-19 | PXD005760 | Pride