Project description:This SuperSeries is composed of the following subset Series: GSE28617: Function, targets and evolution of Caenorhabditis elegans piRNAs (small RNA-Seq) GSE37432: Function, targets and evolution of Caenorhabditis elegans piRNAs (mRNA) Refer to individual Series
Project description:The movement of repetitive elements in the germline creates widespread genomic alterations and pressure for resolution. Here we show that the Caenorhabditis clade took advantage of two transposon expansions by integrating hundreds of elements into its germline transcriptional network. We find that about one-third of C. elegans germline-specific promoters have been co-opted from CERP2 and CELE2 MITE elements and are regulated by HIM-17, a THAP domain-containing transcription factor related to a transposase. An ancestral CERP2 expansion took place in the common Caenorhabditis ancestor, concurrently with mutations in HIM-17 fixed by positive selection, whereas CELE2 expanded only in C. elegans. Through comparative analyses in C. briggsae, we find conservation as well as species-specific CERP2 co-option. Our work reveals the emergence of a novel transcriptional network driven by TE co-option and its impact on regulatory evolution.
Project description:The movement of repetitive elements in the germline creates widespread genomic alterations and pressure for resolution. Here we show that the Caenorhabditis clade took advantage of two transposon expansions by integrating hundreds of elements into its germline transcriptional network. We find that about one-third of C. elegans germline-specific promoters have been co-opted from CERP2 and CELE2 MITE elements and are regulated by HIM-17, a THAP domain-containing transcription factor related to a transposase. An ancestral CERP2 expansion took place in the common Caenorhabditis ancestor, concurrently with mutations in HIM-17 fixed by positive selection, whereas CELE2 expanded only in C. elegans. Through comparative analyses in C. briggsae, we find conservation as well as species-specific CERP2 co-option. Our work reveals the emergence of a novel transcriptional network driven by TE co-option and its impact on regulatory evolution.
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
the C. elegans metabolic network. This network model
contains 1,273 genes, 623 enzymes, and 1,985 metabolic
reactions and is referred to as iCEL1273. Using flux balance
analysis, we show that iCEL1273 is capable of representing the
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
(wormflux.umassmed.edu) and will enable the unraveling of the
mechanisms by which different macro- and micronutrients
contribute to the animal's physiology.
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.
Project description:The movement of repetitive elements in the germline creates widespread genomic alterations and pressure for resolution. Here we show that the Caenorhabditis clade took advantage of two transposon expansions by integrating hundreds of elements into its germline transcriptional network. We find that about one-third of C. elegans germline-specific promoters have been co-opted from CERP2 and CELE2 MITE elements and are regulated by HIM-17, a THAP domain-containing transcription factor related to a transposase. An ancestral CERP2 expansion took place in the common Caenorhabditis ancestor, concurrently with mutations in HIM-17 fixed by positive selection, whereas CELE2 expanded only in C. elegans. Through comparative analyses in C. briggsae, we find conservation as well as species-specific CERP2 co-option. Our work reveals the emergence of a novel transcriptional network driven by TE co-option and its impact on regulatory evolution.
Project description:The movement of repetitive elements in the germline creates widespread genomic alterations and pressure for resolution. Here we show that the Caenorhabditis clade took advantage of two transposon expansions by integrating hundreds of elements into its germline transcriptional network. We find that about one-third of C. elegans germline-specific promoters have been co-opted from CERP2 and CELE2 MITE elements and are regulated by HIM-17, a THAP domain-containing transcription factor related to a transposase. An ancestral CERP2 expansion took place in the common Caenorhabditis ancestor, concurrently with mutations in HIM-17 fixed by positive selection, whereas CELE2 expanded only in C. elegans. Through comparative analyses in C. briggsae, we find conservation as well as species-specific CERP2 co-option. Our work reveals the emergence of a novel transcriptional network driven by TE co-option and its impact on regulatory evolution.
Project description:The nematode Caenorhabditis elegans offers currently untapped potential for carrying out high-throughput, live-animal screens of low molecular weight compound libraries to identify molecules that target a variety of cellular processes. We previously used a bacterial infection assay in C. elegans to identify 119 compounds that affect host-microbe interactions among 37,214 tested. We subsequently found that one of these small molecules, RPW-24, protects C. elegans from bacterial infection by stimulating the host immune response of the nematode. Using transcriptome profiling, epistasis pathway analyses with C. elegans mutants, and an RNAi screen, we showed that RPW-24 promotes resistance to Pseudomonas aeruginosa infection by inducing the transcription of a remarkably small number of C. elegans genes (~1.3% of all genes) in a manner that partially depends on the evolutionarily-conserved p38 MAP kinase pathway and the transcription factor ATF-7. These data demonstrated that the immunostimulatory activity of RPW-24 is required for its efficacy and define a novel C. elegans-based strategy to identify compounds with activity against antibiotic-resistant bacterial pathogens. Here we present the microarray data that were used to define the genes that are differentially regulated in wild-type nematodes following exposure to RPW-24.
Project description:Pattern recognition of bacterial products by host receptors is essential for pathogen sensing in many metazoans. Caenorhabditis elegans, however, do not utilize canonical pattern recognition receptors to activate innate immunity toward bacterial pathogens. Whether other mechanisms evolved in nematodes to directly sense pathogens is not known. Here, we characterize the first bacterial pattern recognition receptor and its natural ligand in C. elegans. We show that the C. elegans nuclear hormone receptor NHR-86/HNF4 senses phenazine-1-carboxamide (PCN), a metabolite produced by pathogenic strains of Pseudomonas aeruginosa, to activate protective anti-pathogen defenses in the intestine. PCN binds to the ligand binding domain of NHR-86/HNF4, a ligand-gated transcription factor, which engages a transcriptional program in intestinal epithelial cells that promotes metabolism of toxic phenazines to provide protection against P. aeruginosa. These data de-orphan a nuclear hormone receptor and demonstrate that sensing a metabolite signal of bacterial virulence allows nematodes to detect pathogens in its environment that are poised to cause disease.
Project description:The goal of this study was to elucidate genes that are employed by the bacterivorous nematode Caenorhabditis elegans to respond to the emerging nosocomial bacterial pathogen Stenotrophomonas maltophilia.