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497 results for “Caenorhabditis”
Hypoxia-inducible factor induces cysteine dioxygenase and promotes cysteine homeostasis in Caenorhabditis elegans
<p>Dedicated genetic pathways regulate cysteine homeostasis. For example, high levels of cysteine activate cysteine dioxygenase, a key enzyme in cysteine catabolism in most animal and many fungal species. The mechanism by which cysteine dioxygenase is regulated is largely unknown. In an unbiased genetic screen for mutations that activate cysteine dioxygenase (<em>cdo-1</em>) in the nematode <em>C. elegans, </em>we isolated loss-of-function mutations in <em>rhy-1 </em>and <em>egl-9, </em>which encode proteins that negatively regulate the stability or activity of the oxygen-sensing hypoxia-inducible transcription factor (<em>hif-1</em>). EGL-9 and HIF-1 are core members of the conserved eukaryotic hypoxia response. However, we demonstrate that the mechanism of HIF-1-mediated induction of <em>cdo-1 </em>is largely independent of EGL-9 prolyl hydroxylase activity and the von Hippel-Lindau E3 ubiquitin ligase, the classical hypoxia signaling pathway components. We demonstrate that <em>C. elegans cdo-1 </em>is transcriptionally activated by high levels of cysteine and <em>hif-1</em>. <em>hif-1-</em>dependent activation of <em>cdo-1</em> occurs downstream of an H<sub>2</sub>S-sensing pathway that includes <em>rhy-1, cysl-1, </em>and <em>egl-9.</em> <em>cdo-1 </em>transcription is primarily activated in the hypodermis where it is also sufficient to drive sulfur amino acid metabolism. Thus, the regulation of <em>cdo-1 </em>by <em>hif-1 </em>reveals a negative feedback loop that maintains cysteine homeostasis. High levels of cysteine stimulate the production of an H<sub>2</sub>S signal. H<sub>2</sub>S then acts through the <em>rhy-1/cysl-1/egl-9 </em>signaling pathway to increase HIF-1-mediated transcription of <em>cdo-1, </em>promoting the degradation of cysteine via CDO-1.</p>
Automated Dual Olfactory Device for Studying Head/Tail Chemosensation in Caenorhabditis elegans
<p>A microfluidic device for simultaneous delivery of olfactory stimuli to the head and the tail of immobilized C elegans to visualize Calcium activity in the nervous system.</p>
Data from: Caenorhabditis elegans germ granules accumulate hundreds of low translation mRNAs with no systematic preference for germ cell fate regulators
<p>In animals with germ plasm, embryonic germline precursors inherit germ granules, condensates proposed to regulate mRNAs coding for germ cell fate determinants. In <em>C. elegans</em>, mRNAs are recruited to germ granules by MEG-3, a sequence non-specific RNA-binding protein that forms stabilizing interfacial clusters on germ granules. Using fluorescent <em>in situ </em>hybridization, we confirmed that 441 MEG-3-bound transcripts distribute in a pattern consistent with enrichment in germ granules. 13 are related to transcripts reported in germ granules in <em>Drosophila</em> or <em>Nasonia</em>. The majority, however, are low-translation maternal transcripts required for embryogenesis that are not maintained preferentially in the nascent germline. Granule enrichment raises the concentration of certain transcripts in germ plasm but is not essential to regulate mRNA translation or stability. Our findings suggest that only a minority of germ granule-associated transcripts contribute to germ cell fate in <em>C. elegans</em> and that the vast majority function as non-specific scaffolds for MEG-3.</p>
Dissecting the sequential evolution of a selfish mitochondrial genome in Caenorhabditis elegans data
<p>Mitochondrial genomes exist in a nested hierarchy of populations where mitochondrial variants are subject to genetic drift and selection at each level of organization, sometimes engendering conflict between different levels of selection, and between the nuclear and mitochondrial genomes. Deletion mutants in the <em>Caenorhabditis elegans</em> mitochondrial genome can reach high intracellular frequencies despite strongly detrimental effects on fitness. During a mutation accumulation (MA) experiment in <em>C. elegans</em>, a 499 bp deletion in <em>ctb-1</em> rose to 90% frequency within cells while significantly reducing fitness. During the experiment, the deletion-bearing mtDNA acquired three additional mutations in <em>nd5</em>, namely two single insertion frameshift mutations in a homopolymeric run, and a base substitution. Despite an additional fitness cost of these secondary mutations, all deletion-bearing molecules contained the <em>nd5 </em>mutations at the termination of the MA experiment. The presence of mutant mtDNA was associated with increased mtDNA copy-number. Variation in mtDNA copy-number was greater in the MA lines than in a wildtype nuclear background, including a severe reduction in copy-number at one generational timepoint. Evolutionary replay experiments using different generations of the MA experiment as starting points suggests that two of the secondary mutations contribute to the proliferation of the original <em>ctb-1</em> deletion by unknown mechanisms. </p>
Orsay virus infection increases Caenorhabditis elegans resistance to heat-shock
<p>The heat shock response plays a role in the immune defense against viruses across various organisms. Studies on model organisms show that inducing this response prior to viral exposure enhances host resistance to infections, while deficient responses make individuals more vulnerable. Moreover, viruses rely on components of the heat shock response for their own stability and viral infections improve thermal tolerance in plants, giving infected individuals an advantage in extreme conditions, which aids the virus in replication and transmission. Here, we examine the interaction between the nematode Caenorhabditis elegans and its natural pathogen the Orsay virus (OrV) under heat stress. We found that OrV infection leads to differential expression of heat-stress related genes, and infected populations showed increased resistance to heat shock. This resistance correlated with increased expression of argonautes alg-1 and alg-2, which are crucial for survival after heat shock and for OrV replication. Overall, our study suggests an environmental-dependent mutualistic relationship between the nematode and OrV, potentially expanding the animal's ecological niche and providing the virus with extra opportunities for replication and adaptation to extreme conditions.</p>
Comparative genomics of ten new Caenorhabditis species
<p><strong>Phylogenomic analysis</strong></p> <p><code>ASTRAL_species_tree.ASTRAL_branch_lengths.nwk</code>: Species tree generated by ASTRAL-III with branch lengths in coalescent units</p> <p><code>ASTRAL_species_tree.RAxML_branch_lengths.nwk</code>: Species tree generated by ASTRAL-III with branch lengths in substitutions per site as estimated by RAxML (GTR+Γ)</p> <p><code>Caenorhabditis_33species_1988loci_supermatrix.fas</code>: Supermatrix composed of 1988 single-copy loci 27 of 33 species analysed</p> <p><code>Orthogroups.txt</code>: Original orthology clustering file</p> <p><code>PhyloBayes_species_tree.nwk</code>: Species tree generated by PhyloBayes MPI (CAT-GTR+Γ)</p> <p><code>RAxML_species_tree.nwk</code>: Species tree generated by RAxML (GTR+Γ)</p> <p><code>singlecopy_orthologues_redundantseqs_removed.txt</code>: Orthogroups used in analysis, after removing redundant sequences</p> <p><strong>Intron analysis</strong></p> <p><code>Orthogroups_990_0missing_5hetero_paraloguesremoved_withCDSalignments.txt</code>: Single copy orthogroups.txt file (note: this is after removing redundant sequences arising from uncollapsed heterozygosity and removing orthogroups containing paralogues)</p> <p><code>genome_gene_structure_stats.tsv</code>: File containing gene structure and genome size statistics</p> <p><strong>Notch-like receptor analysis</strong></p> <p><code>OG0000658.below700removed.fa</code>: FASTA file of all sequences in orthogroup that were 700 amino acids or longer.</p> <p><code>OG0000658.below700removed.fa.aln</code>: alignment of the above FASTA file</p> <p><code>OG0000658.below700removed.fa_ProSiteProfiles.tsv</code>: InterProScan search results of the above FASTA file using the ProSiteProfiles database (release 2017_09)</p> <p><code>OG0000658.txt</code>: Line from orthology clustering with all (including those below 700 amino acid) sequence IDs</p> <p><code>RAxML_bipartitions.OG0000658.below700removed.nwk</code>: RAxML ML tree of the above alignment file with bootstrap support values</p> <p><code>extract_branch_lengths.py</code>: Python script used to extract branch lengths</p>
Structural variants of 20 wild isolates of Caenorhabditis elegans
<p>20 VCFs of 20 <em>Caenorhabditis elegans</em> wild isolates against VC2010 reference assembly.</p> <p>Reads come Pacific Biosciences sequencing.</p> <p>Alignment was done using ngmlr.</p> <p>Variant calling was done using Sniffles.</p> <p> </p>
Caenorhabditis presence and its association with microbiome and abiotic variables
<p>This file contains data and code for the research of Caenorhabditis presence and its association with microbiome and abiotic variables, Manu van Wing, BSc thesis, University of Amsterdam, 2023. It contains data on the presence of Caenorhabditis nematodes, the composition of the microbial communities at the sampling site, and the temperature, pH and soil water content of the sampling site.</p>
Ether lipid biosynthesis promotes lifespan extension and enables diverse prolongevity paradigms in Caenorhabditis elegans
<p class="MsoNormal">Biguanides, including the world's most prescribed drug for type 2 diabetes, metformin, not only lower blood sugar but also promote longevity in preclinical models. Epidemiologic studies in humans parallel these findings, indicating favorable effects of metformin on longevity and on reducing the incidence and morbidity associated with aging-related diseases. Despite this promise, the full spectrum of molecular effectors responsible for these health benefits remains elusive. Through unbiased screening in <em>C. elegans</em>, we uncovered a role for genes necessary for ether lipid biosynthesis in the favorable effects of biguanides. We demonstrate that biguanides prompt lifespan extension by stimulating ether lipid biogenesis. Loss of the ether lipid biosynthetic machinery also mitigates lifespan extension attributable to dietary restriction, target of rapamycin (TOR) inhibition, and mitochondrial electron transport chain inhibition. A possible mechanistic explanation for this finding is that ether lipids are required for activation of longevity-promoting, metabolic stress defenses downstream of the conserved transcription factor <em>skn-1/</em>Nrf. In alignment with these findings, overexpression of a single, key, ether lipid biosynthetic enzyme, <em>fard-1</em>/FAR1, is sufficient to promote lifespan extension. These findings illuminate the ether lipid biosynthetic machinery as a novel therapeutic target to promote healthy aging.</p>
Data from: Caenorhabditis elegans germ granules accumulate hundreds of low translation mRNAs with no systematic preference for germ cell fate regulators
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Dissecting the sequential evolution of a selfish mitochondrial genome in Caenorhabditis elegans data
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Data from: A novel sperm-derived seminal fluid protein in Caenorhabditis nematodes
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Cumulative effects of mutation and selection on susceptibility to bacterial pathogens in <em>Caenorhabditis elegans</em>
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Orsay virus infection increases Caenorhabditis elegans resistance to heat-shock
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Short-term heritable variation overwhelms two hundred generations of mutational variance for metabolic traits in Caenorhabditis elegans
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Transgenerational fitness effects of lifespan extension by dietary restriction in Caenorhabditis elegans
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Evolutionary changes of non-coding elements associated with transition of sexual mode in Caenorhabditis nematodes
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Hypoxia-inducible factor induces cysteine dioxygenase and promotes cysteine homeostasis in Caenorhabditis elegans
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Ether lipid biosynthesis promotes lifespan extension and enables diverse prolongevity paradigms in Caenorhabditis elegans
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Data from: Dauer life stage of Caenorhabditis elegans induces elevated levels of defense against the parasite Serratia marcescens
Host-parasite research often focuses on a single host life stage, yet different life stages may exhibit different defenses. The nematode Caenorhabditis elegans has an alternate dispersal life stage, dauer. Despite dauer's importance in nature, we know little of how it responds to parasites. Previous research indicates that non-dauer C. elegans prefer to consume the virulent bacterial parasite, Serratia marcescens, when given a choice between the parasite and benign Escherichia coli. Here, we compared the preferences of dauer individuals from six strains of C. elegans to the preferences of other life stages. We found that dauer individuals exhibited reduced preference for S. marcescens, and dauers from some strains preferred E. coli to S. marcescens. In addition to testing food preference, a mechanism of parasite avoidance, we also measured host mortality rates after direct parasite exposure to determine if life stage also altered host survival. Overall, dauer individuals exhibited reduced mortality rates. However, dauer versus non-dauer larvae mortality rates also varied significantly by host strain. Collectively, we found evidence of dauer-induced parasite avoidance and reduced mortality in the presence of a parasite, but these effects were strain-specific. These results demonstrate the importance of host life stage and genotype when assessing infection dynamics.
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