Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcriptional profiling of nhr-114 vs. glp-1 animals, and wild type + Trp vs. wild type animals.

ABSTRACT: 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.

ORGANISM(S): Caenorhabditis elegans

SUBMITTER: Xicotencatl Gracida

PROVIDER: E-GEOD-43864 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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. 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).

Dataset Information

Transcriptional profiling of nhr-114 vs. glp-1 animals, and wild type + Trp vs. wild type animals.

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