Ontology highlight
ABSTRACT:
PROVIDER: PRJNA547370 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9208170_1.fastq.gz | Fastqsanger.gz | |||
| SRR9208170_2.fastq.gz | Fastqsanger.gz | |||
| SRR9208171_1.fastq.gz | Fastqsanger.gz | |||
| SRR9208171_2.fastq.gz | Fastqsanger.gz | |||
| SRR9208172_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:The RpoN-RpoS alternative sigma factor pathway is essential for key adaptive responses by Borrelia burgdorferi, particularly those involved in the infection of a mammalian host. A putative response regulator, Rrp2, ostensibly is required for activation of the RpoN-dependent transcription of rpoS. However, questions remain regarding the extent to which the three major constituents of this pathway (Rrp2, RpoN, and RpoS) act interdependently. To assess the functional interplay between Rrp2, RpoN, and RpoS, we employed microarray analyses to compare gene expression levels in rrp2, rpoN, or rpoS mutants of parental strain 297. We identified 98 genes that were similarly regulated by Rrp2, RpoN and RpoS, and an additional 47 genes were determined to be likely regulated by this pathway. The substantial overlap between genes regulated by RpoS and RpoN provides compelling evidence that these two alternative sigma factors form a congruous pathway and that RpoN regulates B. burgdorferi gene expression through RpoS. Although several known B. burgdorferi virulence determinants were regulated by the RpoN-RpoS pathway, a defined function has yet to be ascribed to most of the genes substantially regulated by Rrp2, RpoN and RpoS, therefore providing additional avenues for future research into the genetic determinants contributing to virulence expression by B. burgdorferi. Keywords: gene profiling 297 (wt) vs rpoS mutant: 6 slides, 12 hybridizations (including dyeswaps), three biological replicates 297 (wt) vs rpoN mutant: 5 slides, 10 hybridizations (including dyeswaps), three biological replicates 297 (wt) vs rrp2 mutant: 6 slides, 12 hybridizations (including dyeswaps), three biological replicates 5A18 (wt) vs XY424.3 (rrp2 mutant): 5 slides, 10 hybridizations (including dyeswaps), three biological replicates 297 (wt) vs rpoS mutant: 6 slides, 12 hybridizations (including dyeswaps), three biological replicates 297 (wt) vs rpoN mutant: 5 slides, 10 hybridizations (including dyeswaps), three biological replicates 297 (wt) vs rrp2 mutant: 6 slides, 12 hybridizations (including dyeswaps), three biological replicates 5A18 (wt) vs XY424.3 (rrp2 mutant): 5 slides, 10 hybridizations (including dyeswaps), three biological replicates
2008-09-09 | E-GEOD-11284 | biostudies-arrayexpress
Project description:The RpoN-RpoS alternative sigma factor pathway is essential for key adaptive responses by Borrelia burgdorferi, particularly those involved in the infection of a mammalian host. A putative response regulator, Rrp2, ostensibly is required for activation of the RpoN-dependent transcription of rpoS. However, questions remain regarding the extent to which the three major constituents of this pathway (Rrp2, RpoN, and RpoS) act interdependently. To assess the functional interplay between Rrp2, RpoN, and RpoS, we employed microarray analyses to compare gene expression levels in rrp2, rpoN, or rpoS mutants of parental strain 297. We identified 98 genes that were similarly regulated by Rrp2, RpoN and RpoS, and an additional 47 genes were determined to be likely regulated by this pathway. The substantial overlap between genes regulated by RpoS and RpoN provides compelling evidence that these two alternative sigma factors form a congruous pathway and that RpoN regulates B. burgdorferi gene expression through RpoS. Although several known B. burgdorferi virulence determinants were regulated by the RpoN-RpoS pathway, a defined function has yet to be ascribed to most of the genes substantially regulated by Rrp2, RpoN and RpoS, therefore providing additional avenues for future research into the genetic determinants contributing to virulence expression by B. burgdorferi. Keywords: gene profiling
2008-09-09 | GSE11284 | GEO
Project description:The alternative sigma factor RpoS plays a central role in the critical host-adaptive response of the Lyme disease spirochete, Borrelia burgdorferi. We previously identified bbd18 as a negative regulator of RpoS but could not inactivate bbd18 in wild-type spirochetes. In the current study we employed an inducible bbd18 gene to demonstrate the essential nature of BBD18 for viability of wild-type spirochete viability in vitro and at a unique point in vivo. Transcriptomic analyses of BBD18 depleted cells demonstrated global induction of RpoS-dependent genes prior to lysis, with the absolute requirement for BBD18, both in vitro and in vivo, circumvented by deletion of rpoS. The increased expression of plasmid prophage genes and the presence of phage particles in the supernatants of lysing cultures indicate that RpoS regulates phage lysis-lysogeny decisions. Through this work we identify a mechanistic link between endogenous transducing prophages and the RpoS-dependent adaptive response of the Lyme disease spirochete. The alternative sigma factor RpoS plays a central role in the critical host-adaptive response of the Lyme disease spirochete, Borrelia burgdorferi. We previously identified bbd18 as a negative regulator of RpoS but could not inactivate bbd18 in wild-type spirochetes. In the current study we employed an inducible bbd18 gene to demonstrate the essential nature of BBD18 for viability of wild-type spirochete viability in vitro and at a unique point in vivo. Transcriptomic analyses of BBD18 depleted cells demonstrated global induction of RpoS-dependent genes prior to lysis, with the absolute requirement for BBD18, both in vitro and in vivo, circumvented by deletion of rpoS. The increased expression of plasmid prophage genes and the presence of phage particles in the supernatants of lysing cultures indicate that RpoS regulates phage lysis-lysogeny decisions. Through this work we identify a mechanistic link between endogenous transducing prophages and the RpoS-dependent adaptive response of the Lyme disease spirochete.
2022-12-12 | PXD037736 | Pride
Project description:Our study is the first to demonstrate BadR as a repressor of rpoS and thus facilitates spirochete’s transition back into ticks. BadR binds upstream and represses rpoS in unfed ticks. GLcNA-6P, an abundant nutrient of blood and released by subsequent remodeling of the tick peritrophic membrane, relieves repression of BadR on rpoS facilitating vertebrate host adaptation. BadR regulates chitobiose utilization genes and activates genes critical for spirochetes residence of ticks (lp28-4 genes) badR-deficient strain (Gene BB0693) compared to B31-A3 parental wild-type B. burgdorferi strains
2013-02-22 | GSE38827 | GEO
Project description:Borrelia burgdorferi, the etiological agent of Lyme disease, persists in nature through an enzootic cycle consisting of a vertebrate host and an Ixodes tick vector. The sequence motifs modified by two well-characterized restriction/modification loci of B. burgdorferi type strain B31 were recently described, but the methylation profiles of other Lyme disease Borrelia have not been characterized. Herein, the methylomes of B. burgdorferi type strain B31 and 7 clonal derivatives, along with B. burgdorferi N40, B. burgdorferi 297, B. burgdorferi CA-11, B. afzelii PKo, B. afzelii BO23, and B. garinii PBr, were defined through PacBio SMRT sequencing. This analysis revealed 9 novel sequence motifs methylated by the plasmid-encoded restriction/modification enzymes of these Borrelia strains. Furthermore, while a previous analysis of B. burgdorferi B31 revealed an epigenetic impact of methylation on the global transcriptome, the current data contradict those findings; our analyses of wild-type B. burgdorferi B31 revealed no consistent differences in gene expression among isogenic derivatives lacking one or more restriction/modification enzyme(s).
2021-03-24 | GSE169460 | GEO
Project description:Lyme disease is a result from an infection by the spirochete Borrelia burgdorferi, and is the leading vector-borne disease in North America. Due to the genomic and proteomic variability of different B. burgdorferi isolates, the study and further comparison of their proteome is key to understand the biology and infectivity of these spirochetes. Mass spectrometry-based proteomics was used to assemble peptide datasets of laboratory isolates B31, MM1, B31-ML23, and the infective isolates B31-5A4, B31-A3, and 297, as well as other public datasets, and is publicly available as the Borrelia PeptideAtlas (http://www.peptideatlas.org/builds/borrelia/). These datasets include information on total proteome, secretome, and membrane proteome of the B. burgdorferi.
2024-09-03 | PXD046281 | Pride
Project description:B. burgdorferi isolates differ in pathogenicity, and a correlation between RST type and pathogenicity was observed: the most invasive of the isolates are associated with RST1 and the least invasive with RST3 (Wang et al. 2001, Wang et al. 2002, Wormser et al. 1999). Comparative genome hybridization employing custom B. burgdorferi 70mer oligonucleotide microarrays representing all reference strain B31MI ORFs was used to assess genome plasticity, to reveal genes that are conserved and thus may encode essential functions and to reveal elements encoding potential virulence factors in 15 B. burgdorferi isolates (B479, B515, BL206, 297, B376, B379, BL224, B331, B348, B356, B408, B418, B500, JD1, N40) representing all three RST types. Total genomic DNA for each isolate was labeled with cy3 and hybridized simultaneously with cy5-labeled B31MI DNA as reference. Each hybridization was performed in duplicate.<br> Microarray quality was determined by preliminary hybridizations with reference B31MI DNA labeled with both cy3 and cy5. The specificity of the arrays was assessed by cohybridization of cy-3 labeled DNA from strain B314, a B31 derivative lacking linear plasmids (Sadziene et al. 1993), with cy5-labeled B31MI DNA.
2006-08-15 | E-MEXP-735 | biostudies-arrayexpress
Project description:The bacterial stringent response is triggered by deficiencies of available nutrients andother environmental stresses. It is mediated by 5'-triphosphate-guanosine-3'- diphosphate and 5'-diphosphate-guanosine-3'-diphosphate (collectively (p)ppGpp) and generates global changes in gene expression and metabolism that enable bacteria to adapt to and survive these challenges. Borrelia burgdorferi encounters multiple stressors in its cycling between ticks and mammals that could trigger the stringent response. We have previously shown that the B. burgdorferi stringent response is mediated by a single enzyme, RelBbu, with both (p)ppGpp synthase and hydrolase activities, and that a B. burgdorferi 297 relBbu null deletion mutant was defective in adapting to stationary phase, incapable of down-regulating synthesis of rRNA and could not infect mice. We have now used this deletion mutant and microarray analysis to identify genes comprising the rel regulon in B. burgdorferi cultured at 34°C, and found that transcription of genes involved in glycerol metabolism is induced by relBbu. Culture of the wild-type parental strain, the relBbu deletion mutant and its complemented derivative at 34°C and 25°C in media containing glucose or glycerol as principal carbon sources revealed a growth defect in the mutant, most evident at the lower temperature. Transcriptional analysis of the glp operon for glycerol uptake and metabolism in these three strains confirmed that relBbu was necessary and sufficient to increase transcription of this operon in the presence of glycerol at both temperatures, and particularly at 25°C. These results confirm and extend previous findings regarding the stringent response in B. burgdorferi. They also demonstrate that the stringent response regulates glycerol metabolism in this organism and is likely crucial for its optimal growth in ticks.
2015-01-30 | E-MTAB-3029 | biostudies-arrayexpress
Project description:Purpose: Studies on gene expression changes in joint and heart tissues of laboratory mice have provided insights into the localized host responses to Borrelia burgdorferi colonization; however, gene expression changes in the CNS of mice during B. burgdorferi infection remain unclear. Therefore, we took an unbiased approach to examine potential changes in the dura mater as well as the brain cortex and hippocampus at day 7 post-infection using RNA sequencing (RNA-seq). Methods: Dura mater, brain cortex, and hippocampal mRNA profiles of 6-8 week old C3H/HeN mice infected with B. burgdorferi strain 297 or mock infected (n=4 per group) were generated by paired-end sequencing using the Illumina HiSeq 4000. The sequence reads were aligned using STAR aligner followed by DESeq2 for differential expression analysis. qRT–PCR validation was performed using SYBR Green assays. Results: In the dura mater, the presence of B. burgdorferi is associated with upregulation of genes consistent with TLR/NF-κB signalling and associated inflammatory cytokines and chemokines in addition to upregulation of interferon stimulated genes. In contrast, the brain parenchyma exhibits mainly an increase in interferon stimulated genes in response to B. burgdorferi infection without an associated cytokine response. Conclusion: Overall, the findings reported in this study are significant, as the lack of a tractable animal model has hindered our understanding of host-pathogen interactions in the CNS. Our results describe a model system that will allow for future studies evaluating the bacterial, host, and environmental factors that can contribute to the severity of CNS involvement during B. burgdorferi infection, as well as evaluating potential novel prophylactic and therapeutic interventions for this important disease.
2021-01-22 | GSE149287 | GEO