Ontology highlight
ABSTRACT:
PROVIDER: PRJNA734749 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Contains both of the known virulence plasmids of Bacillus anthracis.
| PRJNA17709 | ENA
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis). We are working with an enzyme able to directly transfer sialyl residues among macromolecules known as the trans-sialidase. It constitutes a virulence factor from Trypanosoma cruzi, the agent of the Chagas' Disease the American trypanosomiasis. We described the ability of this virulence factor to induce thymocyte apoptosis in vivo that happens after silayl residue mobilization. The apoptosis is mediated by the thymic epithelial cells in the nurse cell complex. By employing the microarray approach we wish to analyze the gene expression induced in the thymus after TS treatment. Examination of differential expression in thymocytes between male and female mice of genes related to glycosylation. RNA samples (in triplicate) purified from thymocytes were analyzed by Glyco-gene Chip analysis.
2011-02-04 | E-GEOD-27054 | biostudies-arrayexpress
Project description:Many species of pathogenic bacteria harbor critical plasmid-encoded virulence factors, and yet the regulation of plasmid replication is often poorly understood despite playing key role in plasmid-encoded gene expression. Human pathogenic Yersinia, including the plague agent Yersinia. pestis and its close relative Y. pseudotuberculosis, require the type III secretion system (T3SS) virulence factor to subvert host defense mechanisms and colonize host tissues. The Yersinia T3SS is encoded on the IncFII plasmid for Yersinia virulence (pYV). Several layers of gene regulation enables a large increase in expression of Yersinia T3SS genes at mammalian body temperature. Surprisingly, T3SS expression is also controlled at the level of gene dosage. The number of pYV molecules relative to the number of chromosomes per cell, referred to as plasmid copy number, increases with temperature. The ability to increase and maintain elevated pYV plasmid copy number, and therefore T3SS gene dosage, at 37˚C is important for Yersinia virulence. In addition, pYV is highly stable in Yersinia at all temperatures, despite being dispensable for growth outside the host. Yet how Yersinia reinforces elevated plasmid replication and plasmid stability remains unclear. In this study, we show that the chromosomal gene pcnB encoding the polyadenylase PAP I is required for regulation of pYV plasmid copy number (PCN), maintenance of pYV in the bacterial population outside the host, robust T3SS activity, and Yersinia virulence in a mouse infection model. Likewise, pcnB/PAP I is also required for robust expression of the Shigella flexneri virulence plasmid-encoded T3SS that, similar to Yersinia, is encoded on a virulence plasmid whose replication is regulated by sRNA. Furthermore, Yersinia and Shigella pcnB/PAP I is required for maintaining normal PCN of model antimicrobial resistance (AMR) plasmids whose replication is regulated by sRNA, thereby increasing antibiotic resistance by ten-fold. These data suggest that pcnB/PAP I contributes to the spread and stabilization of sRNA-regulated virulence and AMR plasmids in bacterial pathogens, and is essential in maintaining the gene dosage required to mediate plasmid-encoded traits. Importantly pcnB/PAP I has been bioinformatically identified in many species of bacteria despite being studied in only a few species to date. Our work highlights the potential importance of pcnB/PAP I in antibiotic resistance, and shows for the first time that pcnB/PAP I reinforces PCN andpromotes virulence plasmid stability in natural pathogenic hosts with a direct impact on bacterial virulence.
2025-03-20 | GSE292107 | GEO
Project description:Background: Enterohemorrhagic Escherichia coli (EHEC) O157 causes severe food-bone illness in humans. The chromosome of O157 consists of 4.1-Mb backbone sequences shared by benign E. coli K-12, and 1.4-Mb O157-specific sequences encoding many virulence determinants such as Shiga toxin genes (stxs) and the locus of enterocyte effacement (LEE). Non-O157 EHECs belonging to clonal lineages distinct from O157 also cause similar illness in humans. According to the parallel evolution model, they have independently acquired the major virulence determinants, stxs and LEE. However, the genomic differences between O157 and non-O157 EHECs have not yet systematically been analyzed. Results: By using the microarray and Whole Genome PCR scanning analyses, we performed a whole genome comparison of 20 EHEC strains of O26, O111, and O103 serotypes with O157. In non-O157 EHEC strains, although genome sizes were similar with or rather larger than O157 and the backbone regions were well conserved, O157-specific regions were very poorly conserved. Only around 20% of the O157-specific genes were fully conserved in each non-O157 serotype. However, the non-O157 EHECs contained a significant number of virulence genes found on prophages and plasmids in O157, and also multiple prophages similar but significantly divergent from those in O157. Conclusion: Although O157 and non-O157 EHECs have independently acquired a huge amount of serotype- or strain-specific genes by lateral gene transfer, they share an unexpectedly large number of virulence genes. Independent infections of similar but distinct bacteriophages carrying these virulence determinants appear to be involved in the parallel evolution of EHEC. Keywords: comparative genomic hybridization, CGH
2007-08-23 | GSE7931 | GEO
Project description:Plasmids were constructed harboring protospacers that are perfect targets for spacers #4 and #21 of the array, but contain NNN (all possible PAM combinations) immediately upstream of the protospacer. The plasmids were introduced into V. cholerae with or without a functional CRISPR-cas system and cells were plated on selective media. Cells were collected and the protospacer plasmids were sequenced in a high throughput manner. PAMs were counted using a custom python script
2024-05-06 | E-MTAB-14044 | biostudies-arrayexpress
Project description:We compared the binding patterns in embryonic stem cells of KAP1 and KRAB Zinc Finger (KZNF) proteins as well as H3K4me3 DNA under several conditions. Native human stem cells. Mouse stem cells containing a transchromosomic copy of human chromosome 11, with and without the introduction of plasmids containing KRAB Zinc Finger sequences. We show that certain KZNFs are responsible for the repression of certain retrotransposons in embryonic stem cells, preventing their spread across the genome. ChIP-seq of HESCs and mouse TC11 ESCs with ZNF91 plasmids and with empty vector plasmids. ChIP of KAP1, ZNF486, H3K4me3. At least 2 replicates of each condition.
2014-09-29 | E-GEOD-60210 | biostudies-arrayexpress
Project description:Anthrax is a zoonotic infection caused by the bacterium Bacillus anthracis (BA), a gram-positive, aerobic, spore-forming bacterium that can be misused as a biowarfare agent. The major patho-genicity factors of BA are encoded by genes located on two extrachromosomal plasmids, which are often targeted for specific identification of this pathogen. However, more recent findings show that these plasmids are not a unique feature of BA but can also occur in other Bacillus species. Furthermore, BA is a member of the Bacillus cereus group, a subgroup of closely related Bacilli. Due to the high genetic similarity within this group, it is a challenge to distinguish BA from other members of this group. In this study, we investigated if it is possible to identify species-specific and universally applicable marker peptides for BA. For this purpose, we applied a high-resolution mass spectrometry-based approach for 42 BA isolates. Together with the genomic sequencing data and by developing a bioinformatics data evaluation pipeline, which uses a database containing most of the publicly available protein sequences worldwide (UniParc), we were able to identify eleven universal marker peptides unique to BA, which are located on the chromosome and there-fore might overcome known problems like observable loss of plasmids in environmental species, plasmid loss during cultivation in the lab and that the virulence plasmids are not necessarily a unique feature of BA. The identified chromosomally encoded markers in this study could extend the small panel of already existing chromosomal targets and together with targets for the viru-lence plasmids may pave the way to an even more reliable identification of BA using genomics- as well as proteomics-based techniques.
2023-01-05 | PXD036243 | Pride