Project description:The Gram-positive bacterium Clostridium difficile, a leading cause of antibiotic-associated pseudomembranous colitis, has received increasing attention due to a rising incidence of clinical C. difficile infections (CDI). Despite progress understanding bacterial factors that promote CDI-associated morbidity and mortality, many fundamental aspects of C. difficile biology remain to be explored. Compared to other Gram-positive pathogens, little is known about the bacterium’s transcriptome architecture and in particular mechanisms of post-transcriptional control. To close this knowledge gap, we have applied a suite of transcriptome-focused techniques, including transcription start site mapping (dRNA-seq), transcription termination mapping, and Hfq RIP-seq, resulting in a single-nucleotide resolution RNA map of C. difficile strain 630.
2021-07-07 | GSE155167 | GEO
Project description:Genome wide identification of transcription start site in osteoclast
| PRJNA448810 | ENA
Project description:Genome wide identification of transcription start site in osteoclast precursor
Project description:The pathogenic bacterium Clostridioides difficile is a major cause of antibi-otic-associated diarrheal disease. Treatment of the disease is challenging because anti-biotics used for treatment may also perpetuate the conditions that contributed to initial susceptibility. Elucidating the mechanisms of C. difficile/intestinal epithelium interaction is needed to facilitate the development of new therapeutic options. The studies described in this communication demonstrate the development of a tissue culture system that supported the growth of C. difficile in co-culture with a model of the human intestinal epithelium produced from colonoids, organoids derived from human colonic biopsies. Epithelial cell responses to C. difficile included upregulation of CCL20, encoding a chemokine. Glucosylating toxin production by the bacteria was required for upregulation of CCL20. Additionally, bacteria associated with the monolayer in a non-toxin dependent manner. This system will support future investigation of epithelium/C. difficile interac-tions during CDI and identification of mechanisms that drive pathogenesis by C. difficile in the human intestine.
Project description:Gene expression level of Clostridioides difficile (C. difficile) strain R20291 comparing control C. difficile carring pMTL84151 as vector plasmid with C. difficile conjugated with a pMTL84151-03890 gene. Goal was to determine the effects of 03890 gene conjugation on C. difficile strain R20291 gene expression.
Project description:Clostridioides difficile interactions with the gut mucosa are crucial for colonisation and establishment of infection, however key infection events during the establishment of disease are still poorly defined. To better understand the initial events that occur during C. difficile colonisation, we employed a dual RNA-sequencing approach to study the host and bacterial transcriptomic profiles during C. difficile infection in a dual-environment in vitro human gut model. Temporal changes in gene expression were analysed over 3-24h post infection and comparisons were made with uninfected controls.
Project description:Clostridioides difficile, the leading cause of antibiotic-associated diarrhoea worldwide, is a genetically diverse species which can metabolise a number of nutrient sources upon colonising a dysbiotic gut environment. Trehalose, a disaccharide sugar consisting of two glucose molecules bonded by an α 1,1-glycosidic bond, has been hypothesised to be involved in the emergence of C. difficile hypervirulence due to its increased utilisation by the RT027 and RT078 strains. Using RNA-sequencing analysis, we report the identification of a putative trehalose metabolism pathway which is induced during growth in trehalose: this has not been previously described within the C. difficile species. These data demonstrate the metabolic diversity exhibited by C. difficile which warrants further investigation to elucidate the molecular basis of trehalose metabolism within this important gut pathogen.