Caenorhabditis elegans
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ABSTRACT:
PROVIDER: PRJNA213610 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Caenorhabditis elegans variant detection
| PRJNA949382 | ENA
Project description:Contrasting invertebrate immune defense behaviors caused by a single gene, the Caenorhabditis elegans neuropeptide receptor gene npr-1
| PRJNA257404 | ENA
Project description:The nematode Caenorhabditis elegans feeds on microbes in its natural environment. Some of these microbes are pathogenic and thus harmful to C. elegans. To minimize resulting fitness reductions, C. elegans has evolved various defence mechanisms including behavioural responses (e.g. avoidance behaviour) that reduce contact with the infectious microbes. In this study, we characterized the genetic architecture of natural variation in C. elegans avoidance behaviour against the infectious stages of the Gram-positive bacterium Bacillus thuringiensis. We performed an analysis of quantitative trait loci (QTLs) using recombinant inbred lines (RILs) and introgression lines (ILs) generated from a cross of two genetically as well as phenotypically distinct natural isolates N2 and CB4856. The analysis identified several QTLs that underlie variation in the behavioural response to pathogenic and/or non-pathogenic bacteria. One of the candidates is the npr-1 gene. This gene encodes a homolog of the mammalian neuropeptide receptor. Npr-1 was previously indicated to fully contribute to behavioural defence against the Gram-negative bacterium Pseudomonas aeruginosa and food patch-leaving behaviour on Escherichia coli. Interestingly, in our study, npr-1 is not the only gene mediating avoidance behaviour toward Bacillus thuringiensis. Moreover, our functional analyses show that npr-1 alleles appear to influence survival and avoidance behaviour toward Bacillus thuringiensis in exactly the opposite way than toward Pseudomonas aeruginosa. Our findings highlight the role of npr-1 in fine-tuning nematode behaviour in an ecological context depending on the microbe to which C. elegans is exposed. These opposite phenotypes reflect the diversity in innate immunity to pathogens. To understand the mechanism involved in these opposite phenotypes, we carried out a whole-genome transcriptomics study by RNA-Sequencing. This study includes two pathogens: Pseudomonas aeruginosa PA14 and Bacillus thuringiensis B-18247 (BT247), two strains: N2 and npr-1 (ur89), two time points (12 and 24h) and standard lab food E. coli OP50 as control.
2016-03-31 | GSE60063 | GEO
Project description:The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. Two-channel experiment comparing mixed stage sample to mixed stage mixed 50:50 N2,CB4856 common reference
2013-07-30 | E-GEOD-49307 | biostudies-arrayexpress
Project description:Purpose: To uncover immune genes and pathways that are modulated by the GPCR/NPR-15 Methods: RNA was extracted from synchronized L4 stage npr-15(tm12539) and WT animals grown at 20 C using Qiagen extraction kits and following standard methods Results: RNA seq analyses shows enriched and signficant upregulated immune, neuropeptide, synaptic signaling and metabolism genes and pathways that are dependent on NPR-15 Conclusions: Our study uncovered NPR-15 to be modulator of the innate immunity in C. elegans
2024-03-04 | GSE173367 | GEO
Project description:The nematode Caenorhabditis elegans feeds on microbes in its natural environment. Some of these microbes are pathogenic and thus harmful to C. elegans. To minimize resulting fitness reductions, C. elegans has evolved various defence mechanisms including behavioural responses (e.g. avoidance behaviour) that reduce contact with the infectious microbes. In this study, we characterized the genetic architecture of natural variation in C. elegans avoidance behaviour against the infectious stages of the Gram-positive bacterium Bacillus thuringiensis. We performed an analysis of quantitative trait loci (QTLs) using recombinant inbred lines (RILs) and introgression lines (ILs) generated from a cross of two genetically as well as phenotypically distinct natural isolates N2 and CB4856. The analysis identified several QTLs that underlie variation in the behavioural response to pathogenic and/or non-pathogenic bacteria. One of the candidates is the npr-1 gene. This gene encodes a homolog of the mammalian neuropeptide receptor. Npr-1 was previously indicated to fully contribute to behavioural defence against the Gram-negative bacterium Pseudomonas aeruginosa and food patch-leaving behaviour on Escherichia coli. Interestingly, in our study, npr-1 is not the only gene mediating avoidance behaviour toward Bacillus thuringiensis. Moreover, our functional analyses show that npr-1 alleles appear to influence survival and avoidance behaviour toward Bacillus thuringiensis in exactly the opposite way than toward Pseudomonas aeruginosa. Our findings highlight the role of npr-1 in fine-tuning nematode behaviour in an ecological context depending on the microbe to which C. elegans is exposed. These opposite phenotypes reflect the diversity in innate immunity to pathogens. To understand the mechanism involved in these opposite phenotypes, we carried out a whole-genome transcriptomics study by RNA-Sequencing. This study includes two pathogens: Pseudomonas aeruginosa PA14 and Bacillus thuringiensis B-18247 (BT247), two strains: N2 and npr-1 (ur89), two time points (12 and 24h) and standard lab food E. coli OP50 as control. mRNA profiles of wild type (WT) and npr-1 (ur89) C.elegans exposed to either Bacillus thuringiensis B-18247, Pseudomonas aeruginosa PA14 or standard lab food E. coli OP50 at 12h or 24h were generated by deep sequencing, in double or triplicate, using Illumina HiSeq2000.
2016-03-31 | E-GEOD-60063 | biostudies-arrayexpress
Project description:The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food.
2013-07-30 | GSE49307 | GEO
Project description:Temperature is a prominent environmental stimulus that influences life span. Previous studies indicate that in Caenorhabditis elegans, thermosensory perception in the AFD neuron maintains life span at warm temperatures. How thermosensation is translated into neuronal signals that shape aging remains elusive. We found that the Caenorhabditis elegans CREB crh-1, as well as several key genes in AFD thermosensory transduction, were specifically required for normal life span at warm temperatures. crh-1 acted in the AFD to increase transcription of the CRE-containing neuropeptide gene flp-6 in a temperature-dependent manner. Both crh-1 and flp-6 were necessary and sufficient for longevity at warm temperatures, and their effects depended on the AIY interneuron. Moreover, flp-6 signaling downregulated ins-7/insulin and several insulin pathway genes, whose activity compromised life span. We postulate that temperature experience is integrated in the thermosensory neurons to generate CREB-dependent neuropeptide signals that antagonize insulin signaling and promote temperature-specific longevity.
2018-05-01 | GSE68464 | GEO
Project description:This dataset consists of 20 proteomics raw files of two Caenorhabditis elegans strains: N2 and CB4856 under two conditions.
2021-12-28 | MSV000088622 | MassIVE