Ontology highlight
ABSTRACT:
PROVIDER: PRJNA511378 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Squalene makes up 12 % of human skin surface lipids, however little is known about its affects on the host skin microbiome. Here we tested the effect of squalene on genetic regulation of staphylococci, showing that it profoundly affects expression virulence or colonisation determinants, and of iron uptake systems.
2018-06-30 | E-MTAB-6352 | biostudies-arrayexpress
Project description:Xanthomonas is one important model microbe to study the molecular determinants of virulence and host range of pathogens since Xanthomonas is capable of infecting numerous monocotyledonous and dicotyledonous plants. Among the plant diseases caused by Xanthomonas, X. citri subsp. citri (Xcc) causes citrus canker, which has significant impact on citrus production. Xcc is classified into different strains primarily by host range including A and Aw. The A (Asiatic) strain (XccA) has a wide host range and is most virulent, whereas Aw (Wellington) strain has restricted host range including Key or Mexican lime and alemow. We hypothesized that not only gene content but also gene expression contributes to the difference in virulence and host range of closely related strains. To test our hypothesis, comparative genomic and transcriptome analyses were conducted to study the two closely related Xcc A and Aw strains. The genome of X. citri subsp. citri strain Aw12879 (Xcaw) was completely sequenced using 454 Pyrosequencing, Illumina sequencing and Optical mapping. The finished genome (5.3 Mb chromosome and two plasmids pXcaw19 and pXcaw58) of Xcaw was annotated, curated and compared with XccA genome. Protein blast revealed multiple genes including type III secretion system (TIIISS) effectors xopAF and xopAG are present in Xcaw but absent in XccA. Comparative genomic analysis showed various changes in genes encoding LPS and type IV secretion system. Furthermore, RNA-Seq was used to compare expression profile of Xcaw and XccA in nutrient rich (NB) medium and XVM2 medium which is known to mimic the intercellular space of plant cells using Illumina sequencing. Multiple avirulence/effector genes were over-expressed in Xcaw compared to XccA which might contribute to the limited host range of Xcaw compared to XccA. The overexpression of genes involved in cell wall degradation, attachment, ROS (reactive oxygen species) scavenging, nutrient transportation in XccA might contribute to its expanding of host range. Our data suggest that both gene content and gene expression contribute to difference in virulence and host range of bacterial pathogens. This study lays the foundation to further characterize the mechanisms for virulence and host range of strains of X. citri subsp. citri and other bacterial pathogens. mRNA expression profiles of Xcc strain A and Aw were generated in 2 media: NB and XVM2 by deep sequencing, in triplicate, using Illumina GAII.
2013-09-05 | E-GEOD-41519 | biostudies-arrayexpress
Project description:Xanthomonas is one important model microbe to study the molecular determinants of virulence and host range of pathogens since Xanthomonas is capable of infecting numerous monocotyledonous and dicotyledonous plants. Among the plant diseases caused by Xanthomonas, X. citri subsp. citri (Xcc) causes citrus canker, which has significant impact on citrus production. Xcc is classified into different strains primarily by host range including A and Aw. The A (Asiatic) strain (XccA) has a wide host range and is most virulent, whereas Aw (Wellington) strain has restricted host range including Key or Mexican lime and alemow. We hypothesized that not only gene content but also gene expression contributes to the difference in virulence and host range of closely related strains. To test our hypothesis, comparative genomic and transcriptome analyses were conducted to study the two closely related Xcc A and Aw strains. The genome of X. citri subsp. citri strain Aw12879 (Xcaw) was completely sequenced using 454 Pyrosequencing, Illumina sequencing and Optical mapping. The finished genome (5.3 Mb chromosome and two plasmids pXcaw19 and pXcaw58) of Xcaw was annotated, curated and compared with XccA genome. Protein blast revealed multiple genes including type III secretion system (TIIISS) effectors xopAF and xopAG are present in Xcaw but absent in XccA. Comparative genomic analysis showed various changes in genes encoding LPS and type IV secretion system. Furthermore, RNA-Seq was used to compare expression profile of Xcaw and XccA in nutrient rich (NB) medium and XVM2 medium which is known to mimic the intercellular space of plant cells using Illumina sequencing. Multiple avirulence/effector genes were over-expressed in Xcaw compared to XccA which might contribute to the limited host range of Xcaw compared to XccA. The overexpression of genes involved in cell wall degradation, attachment, ROS (reactive oxygen species) scavenging, nutrient transportation in XccA might contribute to its expanding of host range. Our data suggest that both gene content and gene expression contribute to difference in virulence and host range of bacterial pathogens. This study lays the foundation to further characterize the mechanisms for virulence and host range of strains of X. citri subsp. citri and other bacterial pathogens.
2013-09-05 | GSE41519 | GEO
Project description:LysR-type transcriptional regulators (LTTRs) are the most common family of transcriptional regulators found in the opportunistic pathogen Pseudomonas aeruginosa. They are known to regulate a wide variety of virulence determinants and have emerged recently as positive global regulators of pathogenicity in a broad spectrum of serious bacterial pathogens. However, in spite of their key role in modulating expression of key virulence determinants underpinning pathogenic traits associated with the process of infection, surprisingly few were found to be transcriptionally altered in co-culture with host cells. bvlR (PA14_26880) an LTTR of previously unknown function, has been shown to be induced in response to host cells, and was therefore investigated for its potential role in virulence. BvlR expression was found to play a pivotal role in regulation of acute virulence determinants such as type III secretion and exotoxin A production. In contrast, loss of bvlR led to an inability to form tight microcolonies, a key step in biofilm formation in the mucoid lung, although surface attachment was increased. bvlR was also seen to a key role in P.aeruginosa pathogenicity within the acute model of infection, Caenorhabditis elegans. Unusually for LTTRs, BvlR was shown to exert its influence exclusively through the transcriptional repression of 307 genes, including the divergently transcribed gene bvlA. This highlights the importance of BvlR as a previously uncharacterized global virulence regulator in P. aeruginosa with a key role in the transcriptional response underlying the host pathogen interaction. Six samples were analysed in total, three biological replicates of the bvlR mutant and bvlR complemented strains.
2014-12-10 | E-GEOD-51491 | biostudies-arrayexpress
Project description:LysR-type transcriptional regulators (LTTRs) are the most common family of transcriptional regulators found in the opportunistic pathogen Pseudomonas aeruginosa. They are known to regulate a wide variety of virulence determinants and have emerged recently as positive global regulators of pathogenicity in a broad spectrum of serious bacterial pathogens. However, in spite of their key role in modulating expression of key virulence determinants underpinning pathogenic traits associated with the process of infection, surprisingly few were found to be transcriptionally altered in co-culture with host cells. bvlR (PA14_26880) an LTTR of previously unknown function, has been shown to be induced in response to host cells, and was therefore investigated for its potential role in virulence. BvlR expression was found to play a pivotal role in regulation of acute virulence determinants such as type III secretion and exotoxin A production. In contrast, loss of bvlR led to an inability to form tight microcolonies, a key step in biofilm formation in the mucoid lung, although surface attachment was increased. bvlR was also seen to a key role in P.aeruginosa pathogenicity within the acute model of infection, Caenorhabditis elegans. Unusually for LTTRs, BvlR was shown to exert its influence exclusively through the transcriptional repression of 307 genes, including the divergently transcribed gene bvlA. This highlights the importance of BvlR as a previously uncharacterized global virulence regulator in P. aeruginosa with a key role in the transcriptional response underlying the host pathogen interaction.
2014-12-10 | GSE51491 | GEO
Project description:The highly pathogenic avian influenza (HPAI) H5N1 viruses continue to circulate in nature and threaten public health. Although several viral determinants and host factors that influence the virulence of HPAI H5N1 viruses in mammals have been identified, the detailed molecular mechanism remains poorly defined and requires further clarification. In our previous studies, we characterized two naturally isolated HPAI H5N1 viruses that had similar viral genomes but differed substantially in their lethality in mice. Here, we explored the molecular determinants and potential mechanism for this difference in virulence. By using reverse genetics, we found that a single amino acid at position 158 of the hemagglutinin (HA) protein substantially affected the systemic replication and pathogenicity of these H5N1 influenza viruses in mice. We further found that the G158N mutation introduced an N-linked glycosylation at sites 158–160 of the HA protein and that this N-linked glycosylation enhanced viral productivity in infected mammalian cells and induced stronger host immune and inflammatory responses to viral infection. These findings further our understanding of the determinants of pathogenicity of H5N1 viruses in mammals.
2016-12-22 | GSE89246 | GEO
Project description:The eukaryotic GID/CTLH complex is a highly conserved E3 ubiquitin ligase involved in a broad range of biological processes. However, a role of this complex in host antimicrobial defenses has not been described. We exploited Mycobacterium tuberculosis (Mtb) induced cytotoxicity in macrophages in a FACS based CRISPR genetic screen to identify host determinants of intracellular Mtb growth restriction. Our screen identified 5 (GID8, YPEL5, WDR26, UBE2H, MAEA) of the 10 predicted members of the GID/CTLH complex as determinants of intracellular growth of both Mtb and Salmonella serovar Typhimurium. We show that the antimicrobial properties of the GID/CTLH complex knockdown macrophages are mediated by enhanced GABAergic signaling, activated AMPK, increased autophagic flux and resistance to cell death. Meanwhile, Mtb isolated from GID/CTLH knockdown macrophages are nutritionally starved and oxidatively stressed. Our study identifies the GID/CTLH complex activity as broadly suppressive of host antimicrobial responses against intracellular bacterial infections.
2024-05-08 | GSE267063 | GEO
Project description:Host genetic determinants of the gut microbiota of wild mice
| PRJEB32701 | ENA
Project description:Members of the genus Vibrio include many pathogens of humans and marine animals that share genetic information via horizontal gene transfer. Hence, the Vibrio pan-genome carries the potential to establish new pathogenic strains by sharing virulence determinants, many of which have yet to be characterized. Here, we investigated the virulence properties of Vibrio proteolyticus, a Gram-negative marine bacterium previously identified as part of the Vibrio consortium isolated from diseased corals. We found that V. proteolyticus causes actin cytoskeleton rearrangements followed by cell lysis in HeLa cells in a contact independent manner. In search of the responsible virulence factor involved, we determined the V. proteolyticus secretome. This proteomics approach revealed various putative virulence factors, including active type VI secretion systems and effectors with virulence toxin domains; however, these type VI secretion systems were not responsible for the observed cytotoxic effects. Further examination of the V. proteolyticus secretome led us to hypothesize and subsequently demonstrate that a secreted hemolysin, belonging to a previously uncharacterized clan of the leukocidin superfamily, was the toxin responsible for the V. proteolyticus-mediated cytotoxicity in both HeLa cells and macrophages. Clearly, there remains an armory of yet-to-be discovered virulence factors in the Vibrio pan-genome that will undoubtedly provide a wealth of knowledge on how a pathogen can manipulate host cells.
2016-05-23 | MSV000079754 | MassIVE