Comparison of gene expression profiles between N2 wild-type C. elegans and an nhr-8(hd117) mutant
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
SUBMITTER: Daniel Magner
PROVIDER: E-GEOD-48675 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Acyl-coA synthases (ACSs) produce fatty acyl-CoAs that are used in metabolic and signaling pathways. Metazoans have a large number of ACS genes with differing expression patterns and substrate preferences, but the physiological roles of most ACS genes are unknown. Here, we focused on the C. elegans acyl CoA synthase, ACS-3, which is known to regulate fat uptake and de novo fat synthesis through the conserved nuclear hormone receptor, nhr-25. We performed microarray analysis of acs-3 mutants to elucidate the acs-3-regulated transcription program. This analysis revealed an enrichment among differentially regulated genes of those involved in lipid metabolism, pathogen and wounding responses, and sterol binding genes, among others. As the immunity genes were the most represented gene class, we performed pathogen sensitivity assays to test the phenotypic consequences of this immune gene regulation. Interestingly, acs-3 mutants were hypersensitive to the fungal pathogen D. coniospora, but only mildly sensitive to the bacterial pathogen P. aeruginosa. acs-3 mutation suppressed nhr-25 mutant sensitivity to P. aeruginosa, yet surprisingly microarray analysis of nhr-25(RNAi) animals revealed significant overlap with the acs-3 mutant transcriptome, with an enrichment of pathogen response genes. The upregulation of pathogen response genes in acs-3(ft5) mutants and following nhr-25 reduction-of-function (rf) does not appear to be due to a constitutive osmotic response or defective cuticle barrier, two potential explanations for the acs-3(ft5) and nhr-25(rf) expression of innate immunity genes in the absence of pathogen exposure. Together, these data indicate that ACS-3 promotes resistance to the fungal pathogen, D. coniospora and regulates innate immunity genes through an unknown mechanism. Potential roles for ACS-3 in innate immunity are discussed. We used two-color expression microarrays to compare the transcriptional profiles in two experimental conditions: 1) comparing wild-type (N2) L4 stage larval worms to acs-3(ft5) L4 larval mutant animals; and 2) animals grown to L4 larval stage on bacteria harboring vectors for either control or nhr-25 RNA-interference (RNAi). L4 stage was determined by morphology of the developing vulva. Three biological replicates were used for each experimental condition. Statistically significant changes in gene expression in each experimental were determined using M-bM-^@M-^\linear models for microarray dataM-bM-^@M-^] (limma).
2014-03-21 | E-GEOD-48605 | biostudies-arrayexpress
Project description:NHR-23, a conserved member of the nuclear receptor family of transcription factors, is required for normal development in C. elegans where it plays a critical role in growth and molting. In a search for NHR-23 dependent genes, we performed whole genome comparative expression microarrays on both control and nhr-23 inhibited synchronized larvae. Genes that decreased in response to nhr-23 RNAi included several collagen genes. Unexpectedly, several hedgehog-related genes were also down-regulated after nhr-23 RNAi. A homozygous nhr-23 deletion allele was used to confirm the RNAi knockdown phenotypes and the changes in gene expression. Our results indicate that NHR-23 is a critical coregulator of functionally linked genes involved in growth and molting and reveal evolutionary parallels among the ecdysozoa. Synchronized populations of L1 larvae were plated with two sets of HT115 bacteria, one that had been transformed with the RNAi vector only (L4440 plasmid) and another that had been transformed with a vector targeting nhr-23 (clone 5174) [Proc Natl Acad Sci USA 98 (2001) 7360-7365]. Worms were kept on 2% agarose plates for 21 hr at 20C, collected, and approximately 200ml of worms resuspended in PBS were used in each individual experiment. Total RNA was isolated from frozen pellets using a Mixer-Mill (Miller-Mill 300) following an RNeasy Mini Kit (Qiagen, Germantown, MD) according to manufacturer protocol. Aliquots of cultures used for RNA isolation were kept on nhr-23 RNAi plates to confirm the knockdown phenotypic changes occurred during subsequent molts.
2012-08-29 | E-GEOD-32031 | biostudies-arrayexpress
Project description:Animals can thrive on variable food resources as a result of autonomous processes and beneficial relationships with their gut microbes. Food intake elicits major physiological changes, which are compensated with transient systemic responses that maintain homeostasis in the organism. This integration of external information occurs through cellular sensory elements, such as nuclear receptors, which modulate gene expression in response to specific cues. Given the importance of the germline stem cells (GSCs) for the development of the germ line and the continuity of the species, it is reasonable to assume that GSCs might be shielded from the negative influence of environmental perturbations. To our knowledge, however, there are no mechanisms reported that protect proliferating germ cells from harmful dietary metabolites. Using Caenorhabditis elegans as a model, we report that the somatic activity of the conserved nuclear receptor nhr-114/HNF4 protects GSC divisions and GSC integrity from dietary metabolites. In the absence of nhr-114 and on certain bacterial diets, otherwise somatically normal animals accumulate germ cell division defects during development and become sterile. We find that in nhr-114(-) animals the induction of germline defects and sterility depends on the bacterial metabolic status with respect to the essential amino acid tryptophan. This illustrates an animal-microbe interaction in which somatic nuclear receptor activity preserves the germline by buffering against dietary metabolites, likely through a somatic detoxifying response. Overall, our findings uncover an unprecedented and presumably evolutionary conserved soma-to-germline axis of communication that maintains reproductive robustness on variable food resources. Trasncriptional profiles of adult sterile nhr-114(RNAi) animals were compared to those of sterile glp-1(q224ts) animals. Independently, the transcriptional profiles of wild type animals fed an OP50 diet supplemented with Tryptophan was compared to wild type animals fed a standard OP50 diet.
2013-03-01 | E-GEOD-43864 | biostudies-arrayexpress
Project description:Transcriptional profiling of N2 vs. nhr-8 mutant worms, aiming to identify direct and indirect targets of the nuclear receptor.
2013-08-06 | GSE48675 | GEO
Project description:Transcriptional profiling of C. elegans NHR-49, NHR-66 and NHR-80
2012-03-15 | GSE34856 | GEO
Project description:Transcriptional profiling of C. elegans NHR-49, NHR-66 and NHR-80 Independent data sets were generated for each mutant vs wildtpe comparison: NHR-49 (N=2), NHR-66 (N=3), NHR-80 (N=4)
2012-03-15 | E-GEOD-34856 | biostudies-arrayexpress
Project description:Acyl-coA synthases (ACSs) produce fatty acyl-CoAs that are used in metabolic and signaling pathways. Metazoans have a large number of ACS genes with differing expression patterns and substrate preferences, but the physiological roles of most ACS genes are unknown. Here, we focused on the C. elegans acyl CoA synthase, ACS-3, which is known to regulate fat uptake and de novo fat synthesis through the conserved nuclear hormone receptor, nhr-25. We performed microarray analysis of acs-3 mutants to elucidate the acs-3-regulated transcription program. This analysis revealed an enrichment among differentially regulated genes of those involved in lipid metabolism, pathogen and wounding responses, and sterol binding genes, among others. As the immunity genes were the most represented gene class, we performed pathogen sensitivity assays to test the phenotypic consequences of this immune gene regulation. Interestingly, acs-3 mutants were hypersensitive to the fungal pathogen D. coniospora, but only mildly sensitive to the bacterial pathogen P. aeruginosa. acs-3 mutation suppressed nhr-25 mutant sensitivity to P. aeruginosa, yet surprisingly microarray analysis of nhr-25(RNAi) animals revealed significant overlap with the acs-3 mutant transcriptome, with an enrichment of pathogen response genes. The upregulation of pathogen response genes in acs-3(ft5) mutants and following nhr-25 reduction-of-function (rf) does not appear to be due to a constitutive osmotic response or defective cuticle barrier, two potential explanations for the acs-3(ft5) and nhr-25(rf) expression of innate immunity genes in the absence of pathogen exposure. Together, these data indicate that ACS-3 promotes resistance to the fungal pathogen, D. coniospora and regulates innate immunity genes through an unknown mechanism. Potential roles for ACS-3 in innate immunity are discussed.
2014-03-21 | GSE48605 | GEO
Project description:We identified target genes for NHR-25 by ChIP-seq at L1 stage of C. elegans. Transcription factor genes were tagged with GFP and their expression examined at L1 stage. Since there are no direct target genes known for NHR-25 that can be used for assessment of enrichment efficiency by quantitative PCR (qPCR), we chose to repeat ChIP-seq experiment of another GFP tagged transcription factor, PHA-4 for which the ChIP-seq was performed during a pilot experiment of modENCODE project using the same transgenic strain and antibody (a gift from Tony Hyman lab). pha-4 and nhr-25 transgenic worm were studied in Fed L1 stage.
2013-12-03 | E-GEOD-44710 | biostudies-arrayexpress
Project description:modENCODE_submission_3595 This submission comes from a modENCODE project of Michael Snyder. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We are identifying the DNA binding sites for 300 transcription factors in C. elegans. Each transcription factor gene is tagged with the same GFP fusion protein, permitting validation of the gene's correct spatio-temporal expression pattern in transgenic animals. Chromatin immunoprecipitation on each strain is peformed using an anti-GFP antibody, and any bound DNA is deep-sequenced using Solexa GA2 technology. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-seq. BIOLOGICAL SOURCE: Strain: OP353(official name : OP353 genotype : unc119(ed3);wgIs353(nhr-77::TY1 EGFP FLAG;unc119) outcross : 3 transgene : nhr-77 tags : Bombard tag : GFP::3xFlag description : This strain's transgene was constructed by Mihail Sarov at the Max Planck Institute for Cell Biology in Tubiginen using Tony Hyman's recombineering pipeline. The resulting plasmid was used for biolistic transformation of an unc-119(ed3) strain. The NHR-77::EGFP fusion protein is expressed in the correct nhr-77 spatio-temporal expression pattern. This strain was used for ChIP-seq experiments to map the in vivo binding sites for the NHR-77 transcription factor. made_by : R Waterston ); Developmental Stage: L2; Genotype: unc119(ed3);wgIs353(nhr-77::TY1 EGFP FLAG;unc119); Sex: Hermaphrodite; Transgene: nhr-77; EXPERIMENTAL FACTORS: Developmental Stage L2; Target gene nhr-77; Strain OP353(official name : OP353 genotype : unc119(ed3);wgIs353(nhr-77::TY1 EGFP FLAG;unc119) outcross : 3 transgene : nhr-77 tags : Bombard tag : GFP::3xFlag description : This strain's transgene was constructed by Mihail Sarov at the Max Planck Institute for Cell Biology in Tubiginen using Tony Hyman's recombineering pipeline. The resulting plasmid was used for biolistic transformation of an unc-119(ed3) strain. The NHR-77::EGFP fusion protein is expressed in the correct nhr-77 spatio-temporal expression pattern. This strain was used for ChIP-seq experiments to map the in vivo binding sites for the NHR-77 transcription factor. made_by : R Waterston ); temp (temperature) 20 degree celsius
2012-05-09 | E-GEOD-37880 | biostudies-arrayexpress
Project description:modENCODE_submission_3597 This submission comes from a modENCODE project of Michael Snyder. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We are identifying the DNA binding sites for 300 transcription factors in C. elegans. Each transcription factor gene is tagged with the same GFP fusion protein, permitting validation of the gene's correct spatio-temporal expression pattern in transgenic animals. Chromatin immunoprecipitation on each strain is peformed using an anti-GFP antibody, and any bound DNA is deep-sequenced using Solexa GA2 technology. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-seq. BIOLOGICAL SOURCE: Strain: OP353(official name : OP353 genotype : unc119(ed3);wgIs353(nhr-77::TY1 EGFP FLAG;unc119) outcross : 3 transgene : nhr-77 tags : Bombard tag : GFP::3xFlag description : This strain's transgene was constructed by Mihail Sarov at the Max Planck Institute for Cell Biology in Tubiginen using Tony Hyman's recombineering pipeline. The resulting plasmid was used for biolistic transformation of an unc-119(ed3) strain. The NHR-77::EGFP fusion protein is expressed in the correct nhr-77 spatio-temporal expression pattern. This strain was used for ChIP-seq experiments to map the in vivo binding sites for the NHR-77 transcription factor. made_by : R Waterston ); Developmental Stage: L4; Genotype: unc119(ed3);wgIs353(nhr-77::TY1 EGFP FLAG;unc119); Sex: Hermaphrodite; Transgene: nhr-77; EXPERIMENTAL FACTORS: Developmental Stage L4; Target gene nhr-77; Strain OP353(official name : OP353 genotype : unc119(ed3);wgIs353(nhr-77::TY1 EGFP FLAG;unc119) outcross : 3 transgene : nhr-77 tags : Bombard tag : GFP::3xFlag description : This strain's transgene was constructed by Mihail Sarov at the Max Planck Institute for Cell Biology in Tubiginen using Tony Hyman's recombineering pipeline. The resulting plasmid was used for biolistic transformation of an unc-119(ed3) strain. The NHR-77::EGFP fusion protein is expressed in the correct nhr-77 spatio-temporal expression pattern. This strain was used for ChIP-seq experiments to map the in vivo binding sites for the NHR-77 transcription factor. made_by : R Waterston ); temp (temperature) 20 degree celsius
2012-05-09 | E-GEOD-37882 | biostudies-arrayexpress