Comparison of gene expression profiles between N2 wild-type C. elegans and an nhr-8(hd117) mutant
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE48675 | GEO | 2013/08/06
SECONDARY ACCESSION(S): PRJNA211052
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptional profiling of N2 vs. nhr-8 mutant worms, aiming to identify direct and indirect targets of the nuclear receptor. Seven independent synchronized populations of N2 and nhr-8(hd117) animals were grown from eggs on low cholesterol plates at 25 degrees C until mid-L3 larval stage and collected for microarray RNA expression analysis.
2013-08-06 | E-GEOD-48675 | biostudies-arrayexpress
Project description:Transcriptional profiling of N2 vs. mir-243 worms, aiming to identify direct and indirect targets of the microRNA.
2011-09-16 | GSE20558 | GEO
Project description:Transcriptional profiling of N2 vs. mir-243 worms, aiming to identify direct and indirect targets of the microRNA. N2 and mir-243 young-adult worms grown at 20C were analyzed. Three biological replicates with dye-swaps were performed.
2011-09-15 | E-GEOD-20558 | 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. 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:Transcriptional profiling of C. elegans NHR-49, NHR-66 and NHR-80
2012-03-15 | GSE34856 | GEO
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: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:Transcriptional profiling of C. elegans germline-ablated worms versus unablated intact animals, N2 strain
2013-03-01 | GSE44702 | GEO
Project description:Transcriptional profiling of C. elegans germline-ablated worms versus unablated intact animals, N2 strain
2013-03-01 | GSE44703 | GEO
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