RNA Sequencing of npr-15(tm12539) and wild type (WT) N2 C elegans infected with Staphylococcus aureus for 8 hours
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ABSTRACT:
PROVIDER: PRJNA728679 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14480852_1.fastq.gz | Fastqsanger.gz | |||
| SRR14480852_2.fastq.gz | Fastqsanger.gz | |||
| SRR14480853_1.fastq.gz | Fastqsanger.gz | |||
| SRR14480853_2.fastq.gz | Fastqsanger.gz | |||
| SRR14480854_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: To uncover immune genes and pathways that are modulated by the GPCR/NPR-15 during S. aureus infection Methods: RNA was extracted from synchronized L4 stage npr-15(tm12539) and WT animals grown at 20 C and infected with S. aureus for 8 hours, followed by 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 under infection
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Project description:RNA Sequencing of npr-15(tm12539) and wild type (WT) N2 C elegans
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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.
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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
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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.
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