Next Generation Sequencing and Quantitative Analysis of mRNAs in Caenorhabditis elegans fbxl-5 Mutant Animals
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ABSTRACT:
PROVIDER: PRJNA1044836 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26943561.fastq.gz | Fastqsanger.gz | |||
| SRR26943562.fastq.gz | Fastqsanger.gz | |||
| SRR26943563.fastq.gz | Fastqsanger.gz | |||
| SRR26943564.fastq.gz | Fastqsanger.gz | |||
| SRR26943565.fastq.gz | Fastqsanger.gz |
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Project description:Next Generation Sequencing and Quantitative Analysis of mRNAs in Wild-Type Caenorhabditis elegans Animals Consuming Kombucha Tea-assocaited Microbes
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Project description:Next Generation Sequencing and Quantitative Analysis of mRNAs in Wild Type and ceh-60 Mutant Caenorhabditis elegans
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Project description:This project aims to identify novel RNA binding proteins in the nematode, Caenorhabditis elegans. Since interactions between RNAs and proteins may be transient, these animals were crosslinked with UV light at 254 nm which promotes the covalent link between proteins and RNAs. After this, polyadenylated mRNAs were purified via oligo(dT) coupled to magentic beads under stringent conditions. Finally, samples were subjected to mass spectrometry analysis. To rule out the possibility of RNA-independent binding we also analysed other samples: i) samples digested with RNase one; ii) samples where we performed competition assays with polyadenylic acid
2015-10-26 | PXD002226 | Pride
Project description:The molecular mechanisms that govern the metabolic commitment to reproduction, which often occurs at the expense of the soma, remain poorly understood. We identified the C. elegans F-box protein FBXL-5 as a negative regulator of maternal provisioning of vitellogenin lipoproteins, which mediate the transfer of intestinal lipids to the germline. Mutations in fbxl-5 partially suppress the vitellogenesis defects observed in the heterochronic mutants lin-4 and lin-29, both of which ectopically express fbxl-5 at the adult developmental stage. FBXL-5 functions cell-autonomously to negatively regulate expression of the vitellogenin genes; and consistently, intestinal over-expression of FBXL-5 is sufficient to inhibit vitellogenesis, impair overall lipid homeostasis, and reduce lifespan. Our epistasis analyses suggest that fbxl-5 functions in concert with cul-6, a cullin gene, and the Skp1-related genes skr-3 and skr-5 to regulate vitellogenesis. Additionally, fbxl-5 acts genetically upstream of rict-1, which encodes the core mTORC2 protein Rictor, to govern vitellogenesis. Together, our results reveal an unexpected role for a SCF ubiquitin-ligase complex in controlling intestinal lipid homeostasis by tuning mTORC2 activity.
2023-12-01 | GSE248602 | GEO
Project description:Animals integrate metabolic, developmental, and environmental information before committing key resources to reproduction. In C. elegans, adult animals reallocate key fat stores from intestinal cells to the germline via lipoproteins to promote reproduction. I identified the evolutionarily conserved homeodomain transcription factor CEH-60/PBX as a potent regulator of lipid homeostasis, longevity, and stress response pathways. To gain a comprehensive view of CEH-60 transcriptional activity, I profiled the transcriptomes of ceh-60 mutants by mRNA-Seq and identified genome-wide CEH-60 binding sites by ChIP-Seq. These approaches revealed that several homeostatic pathways are directly controlled by the CEH-60 transcription factor. CEH-60 functions cooperatively with UNC-62/MEIS in the intestine to directly activate lipoprotein genes while simultaneously repressing genes involved in stress responses, including the innate immune and oxidative stress responses. Thus in wild-type animals, CEH-60 serves as a molecular switch that promotes reproduction (i.e., lipoproteins) while repressing stress response and longevity pathways. This study identifies a new key regulator of fat metabolism, longevity, and stress response pathways during normal C. elegans development.
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Project description:Yilmaz2016 - Genome scale metabolic model -
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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
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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.
2016-11-03 | MODEL1604210000 | BioModels
Project description:Kombucha Tea (KT), a fermented tea with roots in traditional Chinese medicine, has surged in worldwide popularity due to its purported health benefits. KT contains a symbiotic culture of yeast and bacterial species, many of which are considered human probiotics. The molecular basis of the health benefits of KT has yet to be thoroughly explored in any animal model. We establishC. elegansas a model to query the molecular interactions between Kombucha-associated microbes (KTM) and the host. We find that worms have an established gut microbiome after consuming a KTM-exclusive diet that mirrors the microbial community found in the fermenting culture. Remarkably, animals consuming KTMs display strikingly reduced lipid levels, yet develop and reproduce similarly toE. coli-fed animals. Critically, consumption of a non-fermenting mix of KT microbial isolates (Kombucha microbe mix) resulted in elevated fat accumulation, suggesting that KTMs do not impair nutrient absorption. To identify the host metabolic pathways altered by KTMs, we performed mRNA-seq on KTM-fed animals, finding widespread changes in lipid metabolism genes. Specifically, we found that three lysosomal lipase genes are significantly upregulated in these animals. These lipases, LIPL-1-3, have been previously shown to promote lipophagy via catabolism of lipid droplets. Consistently, KTM-fed animals display reduced levels of triglycerides and smaller lipid droplet sizes. We propose that KTM-fed animals exhibit a fasting-like metabolic state, even in the presence of sufficient nutrient availability, possibly through induction of lipophagy. Elucidating the host metabolic response to KT consumption will provide unprecedented insight into how this popular fermented beverage may impact human health and inform its use in complementary healthcare plans.
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Project description:Innate immunity, the first line of host defense against pathogens, is tightly regulated both transcriptionally and post-transcriptionally. Here, through global transcriptome and proteome analyses in Caenorhabditis elegans, we uncover a modulation of the expression of secreted innate immunity effector proteins by TENT5, one of a recently described family of cytoplasmic poly(A) polymerases. Direct RNA sequencing revealed that TENT-5 polyadenylates mRNAs with signal peptide-encoding sequences, that are translated at the endoplasmic reticulum. Loss of tent-5 function makes worms more susceptible to bacterial infection. Importantly, we demonstrate that the function of TENT-5 in innate immunity is evolutionarily conserved, as its orthologs, TENT5A and TENT5C are induced during macrophage activation and polyadenylate mRNAs, some of which are of genes orthologous to C. elegans TENT-5 targets. In summary, our study reveals cytoplasmic polyadenylation to be a previously unknown component of the post-transcriptional regulation of innate immunity in animals.
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Project description:To maximize fitness, organisms must appropriately allocate energetic resources between essential cellular processes to maintain homeostasis. The nutritional regulators of energy homeostasis have been studied in detail; however, how developmental signals might impinge on these pathways to govern cellular metabolism is poorly understood. We identified a non-canonical role for Hedgehog (Hh), a classic regulator of development, in maintaining intestinal lipid homeostasis in C. elegans. We find that expression of two Hh ligands, GRD-3 and GRD-4, is controlled by the LIN-29/EGR transcription factor in the hypodermis, where the Hh secretion factor CHE-14/Dispatched also facilitates non-cell autonomous Hh signaling. Using C. elegans, we demonstrate that Hh metabolic regulation does not occur through the canonical Hh transcription factor, TRA-1/GLI, but rather through non-canonical signaling that engages mTOR Complex 2 (mTORC2) in the intestine. Hh mutants display impaired lipid homeostasis, including reduced lipoprotein synthesis and fat accumulation, decreased growth, and upregulation of autophagy factors, mimicking loss of mTORC2. Additionally, we found that Hh inhibits p38 MAPK signaling in parallel to mTORC2 activation and that both pathways act together to modulate of lipid homeostasis. Our findings show a non-canonical role for Hedgehog signaling in lipid metabolism via regulation of core homeostatic pathways and reveal a new mechanism by which developmental timing events govern metabolic decisions.
2024-06-01 | GSE268363 | GEO