Protective microbes alter the transcriptional response of Caenorhabditis elegans nematodes to pathogenic infection
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ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE151731 | GEO | 2021/04/20
REPOSITORIES: GEO
Similar Datasets
Project description:Young adult N2 Caenorhabditis elegans were infected with Enterococcus faecalis or Enterococcus faecium for 8 h to determine the transcriptional host response to each enterococcal species. Analysis of differential gene expression in C. elegans young adults exposed to four different bacteria: heat-killed Escherichia coli strain OP50 (control), wild-type E. faecalis MMH594, wild-type E. faecium E007, or Bacillus subtilis PY79 (sigF::kan). Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Brain-heart infusion agar plates (10 ug/ml kanamycin) were used.
2018-02-14 | GSE95636 | GEO
Project description:Germline-encoded pattern recognition receptors (e.g. Toll-like receptors) play key roles in innate immune activation. However, some metazoans, such as C. elegans, do not have canonical mechanisms of pattern recognition, yet they are able to mount anti-pathogen immune defenses. Here, we demonstrate that a nuclear hormone receptor (NHR), a ligand-gated transcription factor, functions in immune activation and pathogen defense. NHRs have expanded dramatically in C. elegans compared to other metazoans. Because NHRs often function redundantly, it has been challenging experimentally to characterize the biology of individual NHRs. Here, we use genetic epistasis experiments, transcriptome profiling analyses and chromatin immunoprecipitation to show NHR-86 is sufficient to activate protective immune defenses against the bacterial pathogen Pseudomonas aeruginosa. Interestingly, NHR-86 drives the transcription of immune effectors whose basal regulation requires the canonical p38 MAPK PMK-1 immune pathway. However, NHR-86 functions independently of PMK-1 and directly induces the transcription of infection response genes in a manner that confers protection from bacterial infection. Importantly, we found that nhr-86 does control immune gene expression and is necessary for host defense against a different pathogen, Enterococcus faecalis. Our findings characterize an ancient role of an NHR in innate immunity, and suggest that the expansion of the NHR protein family in C. elegans has been fueled in part by the need to activate immune defenses in response to pathogen attack.
2019-01-09 | GSE117719 | GEO
Project description:Germline-encoded pattern recognition receptors (e.g. Toll-like receptors) play key roles in innate immune activation. However, some metazoans, such as C. elegans, do not have canonical mechanisms of pattern recognition, yet they are able to mount anti-pathogen immune defenses. Here, we demonstrate that a nuclear hormone receptor (NHR), a ligand-gated transcription factor, functions in immune activation and pathogen defense. NHRs have expanded dramatically in C. elegans compared to other metazoans. Because NHRs often function redundantly, it has been challenging experimentally to characterize the biology of individual NHRs. Here, we use genetic epistasis experiments, transcriptome profiling analyses and chromatin immunoprecipitation to show NHR-86 is sufficient to activate protective immune defenses against the bacterial pathogen Pseudomonas aeruginosa. Interestingly, NHR-86 drives the transcription of immune effectors whose basal regulation requires the canonical p38 MAPK PMK-1 immune pathway. However, NHR-86 functions independently of PMK-1 and directly induces the transcription of infection response genes in a manner that confers protection from bacterial infection. Importantly, we found that nhr-86 does control immune gene expression and is necessary for host defense against a different pathogen, Enterococcus faecalis. Our findings characterize an ancient role of an NHR in innate immunity, and suggest that the expansion of the NHR protein family in C. elegans has been fueled in part by the need to activate immune defenses in response to pathogen attack.
2019-01-09 | GSE117700 | GEO
Project description:Protective microbes alter the transcriptional response of Caenorhabditis elegans nematodes to pathogenic infection
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Project description:C. elegans has served as a laboratory model organism due to its ease of manipulation and the availability of both forward and reverse genetics. In recent years, efforts to study host-pathogen interactions in C. elegans have increased. For example, analysis of infections by bacteria such as Pseudomonas, Salmonella or Serratia has revealed the existence of innate immune pathways in C. elegans that are also conserved in vertebrates. To date, there has been no natural virus infection reported in C. elegans or C. briggsae. Here we describe evidence of natural virus infection in wild isolates of both C. elegans and C. briggsae. Two highly divergent but related RNA viruses in the family Nodaviridae, tentatively named Orsay nodavirus and Santeuil nodavirus, were detected and their genomes partially sequenced. Infected worm lysates passed through 0.2 um filters could be used to infect uninfected worms, which could be further passaged for many generations. Furthermore, the viruses were subject to processing by the RNAi machinery as evidenced by the detection of virally derived small RNAs. Infection of mutant worms defective in small RNA pathways yielded more robust levels of viral RNA as compared to infection of isogenic N2 reference worms. These data demonstrate that nodaviruses are natural parasites of nematodes in the wild. Further study of the interactions between these viruses and nematodes is likely to provide insight into the natural ecology of nematodes and may reveal novel innate immune mechanisms that respond to viral infection.
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Project description:Traditional treatments for bacterial infection have focused upon directly inhibiting growth of the pathogen. However, an equally important determinant of infection outcome is the host defense response. We previously performed a high-throughput chemical screen to identify small molecules that rescued the nematode Caenorhabditis elegans from infection by Pseudomonas aeruginosa. Over 20 of the hits stimulated host defense gene expression. During in-depth studies of five such molecules using microarray analysis, bioinformatic clustering, and RNAi knockdown of candidate gene targets, we identified PMK-1/p38 MAPK and SKN-1/Nrf2 as two key pathways modulated by these hits. Interestingly, the molecules studied did not depend on a single pathway for ameliorating P. aeruginosa pathogenesis in liquid-based assay, but did rely on the PMK-1/p38 MAPK pathway during a colonization-based infection assay on agar. A subset of these molecules was also protective against Enterococcus faecalis and Staphylococcus aureus. In general, the compounds showed little toxicity against mammalian cells or worms, consistent with their identification in a phenotypic, high-content screen. These molecules possess significant potential for use as tools to study innate immune processes
2020-09-19 | GSE137516 | GEO
Project description:C. elegans has served as a laboratory model organism due to its ease of manipulation and the availability of both forward and reverse genetics. In recent years, efforts to study host-pathogen interactions in C. elegans have increased. For example, analysis of infections by bacteria such as Pseudomonas, Salmonella or Serratia has revealed the existence of innate immune pathways in C. elegans that are also conserved in vertebrates. To date, there has been no natural virus infection reported in C. elegans or C. briggsae. Here we describe evidence of natural virus infection in wild isolates of both C. elegans and C. briggsae. Two highly divergent but related RNA viruses in the family Nodaviridae, tentatively named Orsay nodavirus and Santeuil nodavirus, were detected and their genomes partially sequenced. Infected worm lysates passed through 0.2 um filters could be used to infect uninfected worms, which could be further passaged for many generations. Furthermore, the viruses were subject to processing by the RNAi machinery as evidenced by the detection of virally derived small RNAs. Infection of mutant worms defective in small RNA pathways yielded more robust levels of viral RNA as compared to infection of isogenic N2 reference worms. These data demonstrate that nodaviruses are natural parasites of nematodes in the wild. Further study of the interactions between these viruses and nematodes is likely to provide insight into the natural ecology of nematodes and may reveal novel innate immune mechanisms that respond to viral infection. Two small RNA libraries (18-30 nt) from nodavirus-infected and cured C. elegans wild isolate JU1580 were sequenced on the Illumina Genome Analyzer II platform. Samples were treated with tobacco acid pyrophosphatase to allow cloning of small RNA molecules with 5'-triphosphates. Each sample was labelled with a unique four base pair barcode and libraries were multiplexed together with a third library (not included in this submission). The multiplexed libraries were sequenced in triplicate.
2011-01-01 | E-GEOD-21736 | biostudies-arrayexpress
Project description:Host-microbe associations underlie many key processes of host development, immunity, and life history. Yet, none of the current research on the central model species Caenorhabditis elegans considers the worm’s natural microbiome. Instead, almost all laboratories exclusively use the canonical strain N2 and derived mutants, maintained through routine bleach sterilization in monoxenic cultures with an E. coli strain as food. Here, we characterize for the first time the native microbiome of C. elegans and assess its influence on nematode life history characteristics via transcriptomics.
2019-02-25 | GSE111364 | GEO
Project description:Young adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: response to pathogen infection, innate immunity, host-pathogen interactions
2010-06-12 | GSE21819 | GEO
Project description:Pattern recognition of bacterial products by host receptors is essential for pathogen sensing in many metazoans. Caenorhabditis elegans, however, do not utilize canonical pattern recognition receptors to activate innate immunity toward bacterial pathogens. Whether other mechanisms evolved in nematodes to directly sense pathogens is not known. Here, we characterize the first bacterial pattern recognition receptor and its natural ligand in C. elegans. We show that the C. elegans nuclear hormone receptor NHR-86/HNF4 senses phenazine-1-carboxamide (PCN), a metabolite produced by pathogenic strains of Pseudomonas aeruginosa, to activate protective anti-pathogen defenses in the intestine. PCN binds to the ligand binding domain of NHR-86/HNF4, a ligand-gated transcription factor, which engages a transcriptional program in intestinal epithelial cells that promotes metabolism of toxic phenazines to provide protection against P. aeruginosa. These data de-orphan a nuclear hormone receptor and demonstrate that sensing a metabolite signal of bacterial virulence allows nematodes to detect pathogens in its environment that are poised to cause disease.
2023-02-07 | GSE202258 | GEO