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Unknown,Transcriptomics,Genomics,Proteomics

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B31 vs rrp1 mutant

ABSTRACT: Transcriptional profiling of gene expression between parental strain B31 and rrp1 mutant. Cyclic-di-GMP is a bacterial second messenger that modulates many biological processes. Although its role in bacterial pathogenesis during mammalian infection has been widely recognized, the role of c-di-GMP in pathogen's life cycle in vector hosts is less understood. The enzootic cycle of the Lyme disease pathogen Borrelia burgdorferi involves both a mammalian host and an Ixodes tick vector. The B. burgdorferi genome encodes a single copy of the diguanylate cyclase gene (rrp1), which is responsible for the production of c-di-GMP. To determine the role of c-di-GMP in the life cycle of B. burgdorferi, an Rrp1-deficient B. burgdorferi strain was generated. The rrp1 mutant remains infectious in the mammalian host, but could not survive in the tick vector. To identify the mechanisms of Rrp1 contributing to B. burgdorferi pathogenesis and gene regulation, microarray was employed to compare gene expression profiles between the parental strain B31 and the rrp1 mutant. Two-condition experiment, B31 vs. rrp1 mutant. Biological replicates: 3 B31, 3 rrp1 mutant, independently grown and harvested. One replicate (dye-swap) per array.

ORGANISM(S): Borrelia burgdorferi

SUBMITTER: zhiming ouyang

PROVIDER: E-GEOD-26968 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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B31 vs rrp1 mutant

Project description:Transcriptional profiling of gene expression between parental strain B31 and rrp1 mutant. Cyclic-di-GMP is a bacterial second messenger that modulates many biological processes. Although its role in bacterial pathogenesis during mammalian infection has been widely recognized, the role of c-di-GMP in pathogen's life cycle in vector hosts is less understood. The enzootic cycle of the Lyme disease pathogen Borrelia burgdorferi involves both a mammalian host and an Ixodes tick vector. The B. burgdorferi genome encodes a single copy of the diguanylate cyclase gene (rrp1), which is responsible for the production of c-di-GMP. To determine the role of c-di-GMP in the life cycle of B. burgdorferi, an Rrp1-deficient B. burgdorferi strain was generated. The rrp1 mutant remains infectious in the mammalian host, but could not survive in the tick vector. To identify the mechanisms of Rrp1 contributing to B. burgdorferi pathogenesis and gene regulation, microarray was employed to compare gene expression profiles between the parental strain B31 and the rrp1 mutant.

2013-12-31 | GSE26968 | GEO

Epigenomic landscape of Lyme disease spirochetes reveals novel motifs

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).

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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.

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Transcriptional profiling of the Borrelia burgdorferi bb0647 mutant

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Tandem Mass Tags of Borrelia burgdorferi B31 derivative ML23 and SR0736 sRNA mutant grown in vitro at mammalian-like conditions

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2019-10-02 | MSV000084408 | MassIVE

A host type I interferon response is induced by cytosolic sensing of the bacterial second messenger cyclic-di-GMP

Project description:The innate immune system responds to unique molecular signatures that are widely conserved among microbes but that are not normally present in host cells. Compounds that stimulate innate immune pathways may be valuable in the design of novel adjuvants, vaccines, and other immunotherapeutics.The cyclic dinucleotide cyclic-di-guanosine monophosphate (c-di-GMP) is a recently appreciated second messenger that plays critical regulatory roles in many species of bacteria but is not produced by eukaryotic cells. In vivo and in vitro studies have previously suggested that c-di-GMP is a potent immunostimulatory compound recognized by mouse and human cells. Here we provide evidence that c-di-GMP is sensed in the cytosol of mammalian cells via a novel immunosurveillance pathway. The potency of cytosolic signaling induced by cyclic-di- GMP is comparable to that induced by cytosolic delivery of DNA, and both nucleic acids induce a similar transcriptional profile, including triggering of type I interferons and coregulated genes via induction of TBK1, IRF3, NF-!B and MAP kinases. However, the cytosolic pathway that senses c-di-GMP appears to be distinct from all known nucleic acid-sensing pathways.Our results suggest a novel mechanism by which host cells can induce an inflammatory response to a widely produced bacterial ligand. Three-condition experiment: macrophages transfected with mono-GMP (negative control), double-stranded DNA (positive control), or cyclic-di-GMP (experimental condition). Biological replicates: two, independently treated, harvested, and hybridized to arrays. One replicate per array, except two technical replicates were performed for one of the positive control samples.

2009-07-21 | E-GEOD-16943 | biostudies-arrayexpress

Borrelia burgdorferi gene expression in culture before and after antibody enrichment

Project description:Borrelia burgdorferi, the causative agent of Lyme disease, is transmitted to vertebrate hosts by Ixodes ticks. As it moves from tick to host, B. burgdorferi must adapt to survive in a vastly different environment. During the tick bloodmeal, which lasts several days, B. burgdorferi is primed for mammalian infection, growing increasingly virulent as it senses cues from its surroundings in the tick. This conditioning is dependent on key transcriptional regulators; however, the downstream transcriptional changes occurring inside of the tick that promote B. burgdorferi transmission and infection are poorly understood due to technical difficulties in sequencing the B. burgdorferi transcriptome from inside of ticks. We developed a protocol to enrich and sequence B. burgdorferi from inside the tick, and we measured global transcriptional changes occurring in feeding ticks. We identified 192 genes that change expression twofold over the course of the tick bloodmeal, which were predominantly located on the plasmids of the genome. The majority of the upregulated genes encode proteins found at the cell envelope or proteins of unknown function, including 45 upregulated genes encoding outer surface lipoproteins. These genes that increase during feeding are candidates for future functional studies, which can help identify new targets for methods that aim to control the spread of Lyme disease.

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Tick Adiponectin Receptor-Mediated Phospholipid Metabolism Contributes to Borrelia burgdorferi Colonization

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