Lipoprotein Lpp and L, D-transpeptidases regulate the master regulator of virulence AggR in EAEC
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ABSTRACT:
PROVIDER: PRJNA1187590 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31383023_1.fastq.gz | Fastqsanger.gz | |||
| SRR31383023_2.fastq.gz | Fastqsanger.gz | |||
| SRR31383024_1.fastq.gz | Fastqsanger.gz | |||
| SRR31383024_2.fastq.gz | Fastqsanger.gz | |||
| SRR31383025_1.fastq.gz | Fastqsanger.gz |
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Project description:This study demonstrates that Lpp (Braun’s lipoprotein), and L, D-transpeptidases are required for AggR activation. We found that deletion lpp in EAEC resulted in the downregulation of more than 100 genes involved in transport, metabolism, and virulence. Among those genes, fourteen transcriptional factors, including AggR, were differentially expressed in 042Dlpp.
2025-04-30 | GSE282211 | GEO
Project description:Braun/murein lipoprotein (Lpp) is one of the major outer membrane components of gram-negative bacteria belonging to the enterobacteriaceae family that that is involved in inflammatory responses and septic shock. We previously characterized a delta-lpp isogenic mutant of Yersinia pestis CO92 and found that this mutant was defective in surviving in macrophages and was attenuated in a mouse inhalation model of plague when compared to the highly virulent wild-type (WT) bacterium. To better understand how deletion of the lpp gene might affect Yersinia virulence, we performed global transcriptional profiling of the genes in the WT Y. pestis CO92 and its delta-lpp mutant by using microarrays. The organisms were cultured at both 26 and 37 degrees Celsius to simulate the flea vector and mammalian host environments, respectively. Our data revealed vastly different effects of lpp mutation on the transcriptomes of Y. pestis grown at 37 versus 26°C. While the absence of Lpp resulted mainly in the down-regulation of metabolic genes at 26°C, the Y. pestis CO92 lpp mutant cultured at 37°C exhibited profound alterations in stress response and virulence genes, compared to the WT bacterium. We further investigated one of the stress-related genes (htrA) down-regulated in the lpp mutant relative to WT Y. pestis, as HtrA was previously shown to be important for intracellular survival of Y. enterocolitica in macrophages. Indeed, complementation of the delta-lpp mutant with the htrA gene in trans restored intracellular survival of the Y. pestis lpp mutant. Our results support a role for Lpp in Y. pestis CO92 adapatation to the host environment, possibly via transcriptional activation of htrA.
2010-06-04 | GSE19840 | GEO
Project description:Lipoprotein Particle (LPP) exRNA Profiles Isolated from Plasma
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Project description:In 2011, in Germany, Escherichia coli O104:H4 caused the enterohemorrhagic E. coli (EHEC) outbreak with the highest incidence rate of hemolytic uremic syndrome. This pathogen carries an exceptionally potent combination of EHEC- and enteroaggregative E. coli (EAEC)-specific virulence factors. Here, we identified an E. coli O104:H4 isolate that carried a single nucleotide polymorphism (SNP) in the start codon (ATG>ATA) of rpoS, encoding the alternative sigma factor S. The rpoS ATG>ATA SNP was associated with enhanced EAEC-specific virulence gene expression. Deletion of rpoS in E. coli O104:H4 Dstx2 and typical EAEC resulted in a similar effect. Both rpoS ATG>ATA and DrpoS strains exhibited stronger virulence-related phenotypes in comparison to wild type. Using promoter-reporter gene fusions, we demonstrated that wild-type RpoS repressed aggR, encoding the main regulator of EAEC virulence. In summary, our work demonstrates that RpoS acts as a global repressor of E. coli O104:H4 virulence, primarily through an AggR-dependent mechanism.
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Project description:Direct regulons of the master virulence regulator AtxA of Bacillus anthracis
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Project description:An integrative analysis of human biofluid data in the exRNA Atlas revealed the existence of distinct extracellular RNA cargo types. To gain further insight on the biological nature of these cargo types, we correlated exRNA Atlas cargo profiles with a variety of other RNA-seq profiles. This study focuses on lipoprotein particle (LPP) exRNA profiles obtained via sequential density ultracentrifugation (SD-UC) and fast protein liquid chromatography (FPLC).
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Project description:AtxA, the master virulence regulator of Bacillus anthracis, regulates the expression of three toxins that are required for the pathogenicity of Bacillus anthracis. Recent transcriptome analyses also showed that AtxA affects a large number of genes on both chromosome and plasmid, suggesting its role as a global regulator. Its mechanism of gene regulation nor binding target in vivo was, however, not well understood. In this work, we conducted ChIP-seq for cataloging binding sites of AtxA in vivo and Cappable-seq for catalogging the transcription start sites on the B. anthracis genome. For detected regulons, single knockout strains were constructed and RNA-seq was conducted for each strain.
2021-06-28 | GSE167871 | GEO
Project description:Purpose: In this work, we evaluated the role of two indicative species, Citrobacter werkmanii (CW) and Escherichia albertii (EA), in the virulence of two DEC pathotypes, Shiga toxin-producing (STEC) and enteroaggregative (EAEC) Escherichia coli. Methods: To determine the effect of supernatant obtained from CW and EA cultures in STEC strain 86-24 and EAEC strain 042 gene expression, a RNA-seq analysis was performed. T84 cells were infected with DEC strains in the presence or absence of supernatant from EA and IL-8 secretion was evaluated. The effect of supernatant from EA on the growth and adherence of STEC and EAEC to T84 cells was also evaluated. Finally, we studied the participation of long polar fimbriae (Lpf) in STEC and plasmid-encoded toxin (Pet) in EAEC during DEC infection in the presence of supernatant from EA. Results: RNA-seq analysis revealed that several virulence factors in STEC and EAEC were up-regulated in the presence of supernatants from CW and EA. Interestingly, an increase in the secretion of IL-8 was observed in T84 cells infected with STEC or EAEC in the presence of a supernatant from EA. Similar results were observed with the supernatants obtained from clinical strains of E. albertii. Supernatant from EA had no effect on the growth of STEC and EAEC, or on the ability of these DEC strains to adhere to intestinal epithelial cells. Finally, we found that Pet toxin in EAEC was up-regulated in the presence of a supernatant from EA. In STEC, using mutant strains for Lpf fimbriae, our data suggested that these fimbriae might be participating in the increase of IL-8 induced by STEC on intestinal epithelial cells in the presence of a supernatant from EA. Conclusion:Supernatant obtained from an indicative species of DEC-positive diarrhea could modulate gene expression in STEC and EAEC, and IL-8 secretion induced by these bacteria. These data provide new insights into the effect of gut microbiota species in the pathogenicity of STEC and EAEC.
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Project description:In enteric bacteria, the transcription factor ?E maintains membrane homeostasis by inducing expression of proteins involved in membrane repair and of two small, regulatory RNAs (sRNAs) that downregulate synthesis of abundant membrane porins. Here, we describe the discovery of a third ?E-dependent sRNA, MicL, transcribed from a promoter located within the coding sequence of the cutC gene. MicL is synthesized as a 308 nt primary transcript that is processed to an 80 nt form. Both forms possess features typical of Hfq-binding sRNAs, but surprisingly only target a single mRNA, which encodes the outer membrane lipoprotein Lpp, the most abundant protein of the cell. We show that the copper sensitivity phenotype previously ascribed to inactivation of the cutC gene is actually derived from the loss of MicL and elevated Lpp levels. This observation raises the possibility that other phenotypes currently attributed to protein defects are due to deficiencies in unappreciated regulatory RNAs. We also report that ?E activity is sensitive to Lpp abundance and that MicL and Lpp comprise a new ?E regulatory loop that opposes membrane stress. Together MicA, RybB and MicL allow ?E to repress the expression of all abundant outer membrane proteins in response to stress. 12 samples mRNA-seq data, 2 samples ribosome profiling data. For mRNA-seq data, samples were gathered at the indicated time (in min) after induction of either vector (WT), long (MicL), and short (MicL-S) forms of MicL.
2014-07-17 | E-GEOD-58637 | biostudies-arrayexpress
Project description:In enteric bacteria, the transcription factor σE maintains membrane homeostasis by inducing expression of proteins involved in membrane repair and of two small, regulatory RNAs (sRNAs) that downregulate synthesis of abundant membrane porins. Here, we describe the discovery of a third σE-dependent sRNA, MicL, transcribed from a promoter located within the coding sequence of the cutC gene. MicL is synthesized as a 308 nt primary transcript that is processed to an 80 nt form. Both forms possess features typical of Hfq-binding sRNAs, but surprisingly only target a single mRNA, which encodes the outer membrane lipoprotein Lpp, the most abundant protein of the cell. We show that the copper sensitivity phenotype previously ascribed to inactivation of the cutC gene is actually derived from the loss of MicL and elevated Lpp levels. This observation raises the possibility that other phenotypes currently attributed to protein defects are due to deficiencies in unappreciated regulatory RNAs. We also report that σE activity is sensitive to Lpp abundance and that MicL and Lpp comprise a new σE regulatory loop that opposes membrane stress. Together MicA, RybB and MicL allow σE to repress the expression of all abundant outer membrane proteins in response to stress.
2014-07-17 | GSE58637 | GEO