Expression analysis of C. elegans eat-2; acs-20 and ptr-8 eat-2; acs-20 mutants
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ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE224429 | GEO | 2023/02/11
REPOSITORIES: GEO
Similar Datasets
Project description:Investigation of whole genome gene expression level changes in C. elegans eat-2, acs-20 and eat-2; acs-20 mutant compared to the wild-type N2 strain.
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Project description:Investigation of whole genome gene expression level changes in C. elegans eat-2; acs-22 and eat-2; pmk-1; acs-22 mutant compared to the eat-2 strain.
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Project description:Expression analysis of C. elegans wild-type N2, eat-2, acs-20 and eat-2; acs-20 mutants
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Project description:Expression analysis of C. elegans eat-2, eat-2; acs-22 and eat-2; pmk-1; acs-22 mutants
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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: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).
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Project description:It has been suggested that hydrogen sulfide (H2S) may play a pivotal role in mediating some of these caloric restriction (CR)-associated benefits. We therefore explored whether a novel slow-releasing H2S donor compound, FW1256, mimics CR and reproduces CR-associated effects in normal feeding Caenorhabditis elegans. Using transcriptomics analysis via RNA sequencing, we determined sets of differentially expressed genes (DEG) for FW1256-exposed wild-type C. elegans and eat-2 mutants, a genetic model of CR in C. elegans, relative to unexposed wild-type C. elegans. We found that, while FW1256 affects some of the same downstream genes as eat-2 mutation, global gene expression changes are dissimilar between FW1256-exposed C. elegans and eat-2 mutants, suggesting that novel slow-releasing H2S donor compound, FW1256, does not mimic CR at the transcriptional level.
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Project description:MicroRNAs (miRNAs) are involved in the formation of atherosclerosis. However, the alteration of miRNA profile in epicardial adipose tissue (EAT) during atherosclerosis is still uncovered. In this study, we compared the miRNA expression profiles of EAT from non-coronary atherosclerosis disease (CAD) and CAD patients, and found that 250 miRNAs were differentially expressed in CAD patients, which were associated with metabolism, ECM and inflammation process. Among the top 20 up-regulated miRNAs, we found that the expression levels of miR-200 family members (hsa-miR-200b/c-3p, miR-141-3p and miR-429), which were rich in endothelial cells, were increased in EAT from CAD patients significantly.
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Project description:Investigation of whole genome gene expression level changes in early generation Caenorhabditis elegans Bristol N2 rsd-2 and Bristol N2 rsd-6 single mutants, compared to late-generation strains at 25°C and 20°C
2013-06-01 | GSE40459 | GEO
Project description:Analysis of gene expression in two long-lived daf-2 mutant (mutation in the insulin/IGF-1 receptor) and eat-2 mutant (caloric restriction model), comparison of gene expression profiles of two long-lived mutants provide novel insight into longevity Impaired insulin/IGF-1 signaling (IIS) pathway and caloric restriction (CR) are two well-established interventions to prolong lifespan in worm C. elegans. Although many studies using “-omics” approaches have gained informative knowledges on key longevity regulators in either IIS or CR models, few of those investigated the shared regulators between these two longevity interventions and integrated the messages from different –omics studies. In this study, we aimed to identify key pathways and metabolite fingerprints of longevity shared between the two interventions in worms using a multi-omics integration approach. We collected transcriptomics and metabolomics data from two long-lived mutant worm strains, i.e. daf-2 (impaired IIS pathway) and eat-2 (CR model) and compared with N2 strain. We detected many key pathways that were upregulated at the gene expression level in both long-lived mutants, such as defense response and lipid storage, while synthesis of macromolecules and developmental processes were downregulated at the transcript level. From our polar metabolite analysis, we discovered several shared metabolic features between the two long-lived mutants, including glycerol-3P, adenine, xanthine and AMP. In addition, we detected a lowered amino acid pool and two fatty acid species, C18:0 and C17:1, that behaved similarly in both long-lived mutants. After we integrated transcriptomics and metabolomics data based on the annotations in KEGG, our results highlighted a downregulation of pyrimidine metabolism and upregulation of purine metabolism in both long-lived mutants compared to N2 worms. Overall, our findings point towards the existence of shared metabolic pathways that are important for lifespan extension and provide novel insight of potential regulators and metabolic fingerprints for longevity.
2017-11-20 | GSE106672 | GEO