Ontology highlight
ABSTRACT:
PROVIDER: PRJNA782818 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17032700_1.fastq.gz | Fastqsanger.gz | |||
| SRR17032700_2.fastq.gz | Fastqsanger.gz | |||
| SRR17032701_1.fastq.gz | Fastqsanger.gz | |||
| SRR17032701_2.fastq.gz | Fastqsanger.gz | |||
| SRR17032702_1.fastq.gz | Fastqsanger.gz |
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Project description:Comparison of gene expression profiles of Caenorhabditis elegans fed a complex microbiota (either a synthetic community or in soil) or a standard Escherichia coli diet. We find that immune and digestion genes are up-regulated in C. elegans that were fed a complex microbiota.
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Project description:Caenorhabditis elegans is associated in nature with a species-rich, distinct microbiota, which was characterized only recently. Thus, our understanding of the relevance of the microbiota for nematode fitness is still at its infancy. One major benefit that the intestinal microbiota can provide to its host is protection against pathogen infection. However, the specific strains conferring the protection and the underlying mechanisms of microbiota-mediated protection are often unclear. Here, we identify natural C. elegans microbiota isolates that increase C. elegans resistance to pathogen infection. We show that isolates of the Pseudomonas fluorescens subgroup provide paramount protection from infection with the natural pathogen Bacillus thuringiensis through distinct mechanisms. We found that the P. lurida isolates MYb11 and MYb12 (members of the P. fluorescens subgroup) protect C. elegans against B. thuringiensis infection by directly inhibiting growth of the pathogen both in vitro and in vivo. Using genomic and biochemical analyses, we further demonstrate that MYb11 and MYb12 produce massetolide E, a cyclic lipopeptide biosurfactant of the viscosin group, which is active against pathogenic B. thuringiensis. In contrast to MYb11 and MYb12, P. fluorescens MYb115-mediated protection involves increased resistance without inhibition of pathogen growth and most likely depends on indirect, host-mediated mechanisms. This work provides new insight into the functional significance of the C. elegans natural microbiota and expands our knowledge of bacteria-derived compounds that can influence pathogen colonization in the intestine of an animal.
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Project description:Whole-genome metabolic reconstructions for the model organism Caenorhabditis elegans.
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Project description:Yilmaz2016 - Genome scale metabolic model -
Caenorhabditis elegans (iCEL1273)
This model is described in the article:
A Caenorhabditis elegans
Genome-Scale Metabolic Network Model.
Yilmaz LS, Walhout AJ.
Cell Syst 2016 May; 2(5): 297-311
Abstract:
Caenorhabditis elegans is a powerful model to study
metabolism and how it relates to nutrition, gene expression,
and life history traits. However, while numerous experimental
techniques that enable perturbation of its diet and gene
function are available, a high-quality metabolic network model
has been lacking. Here, we reconstruct an initial version of
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conversion of bacterial biomass into C. elegans biomass
during growth and enables the predictions of gene essentiality
and other phenotypes. In addition, we demonstrate that gene
expression data can be integrated with the model by comparing
metabolic rewiring in dauer animals versus growing larvae.
iCEL1273 is available at a dedicated website
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mechanisms by which different macro- and micronutrients
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This model is hosted on
BioModels Database
and identified by:
MODEL1604210000.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
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