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[
Hermann, Editeurs des Sciences et des Arts. Paris, France.,
2002]
L'espce Caenorhabditis elegans fut dcrite en 1900 Alger par E. Maupas, qui s'intressait son mode de reproduction hermaphrodite. Plus tard, vers le milieu du vingtime sicle, V. Nigon et ses collaboratuers Lyon tudirent les reorganizations cellulaires accompagnant la fecundation et les premiers clivages. J. Brun isola les preiers mutants morpholgiques.
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Nat Rev Mol Cell Biol,
2014]
Many organs contain networks of epithelial tubes that transport gases or fluids. A lumen can be generated by tissue that enwraps a pre-existing extracellular space or it can arise de novo either between cells or within a single cell in a position where there was no space previously. Apparently distinct mechanisms of de novo lumen formation observed in vitro - in three-dimensional cultures of endothelial and Madin-Darby canine kidney (MDCK) cells - and in vivo - in zebrafish vasculature, Caenorhabditis elegans excretory cells and the Drosophila melanogaster trachea - in fact share many common features. In all systems, lumen formation involves the structured expansion of the apical plasma membrane through general mechanisms of vesicle transport and of microtubule and actin cytoskeleton regulation.
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Curr Biol,
2005]
Aurora B kinases play important roles during mitosis in eukaryotic cells; new work in Caenorhabditis elegans has identified the Tousled kinase TLK-1 as a substrate activator of the model nematode''''s Aurora B kinase AIR-2 which acts to ensure proper chromosome segregation during
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Genetics,
2019]
The <b>T</b>arget <b>o</b>f <b>R</b>apamycin (TOR or mTOR) is a serine/threonine kinase that regulates growth, development, and behaviors by modulating protein synthesis, autophagy, and multiple other cellular processes in response to changes in nutrients and other cues. Over recent years, TOR has been studied intensively in mammalian cell culture and genetic systems because of its importance in growth, metabolism, cancer, and aging. Through its advantages for unbiased, and high-throughput, genetic and <i>in vivo</i> studies, <i>Caenorhabditis elegans</i> has made major contributions to our understanding of TOR biology. Genetic analyses in the worm have revealed unexpected aspects of TOR functions and regulation, and have the potential to further expand our understanding of how growth and metabolic regulation influence development. In the aging field, <i>C. elegans</i> has played a leading role in revealing the promise of TOR inhibition as a strategy for extending life span, and identifying mechanisms that function upstream and downstream of TOR to influence aging. Here, we review the state of the TOR field in <i>C. elegans</i>, and focus on what we have learned about its functions in development, metabolism, and aging. We discuss knowledge gaps, including the potential pitfalls in translating findings back and forth across organisms, but also describe how TOR is important for <i>C. elegans</i> biology, and how <i>C. elegans</i> work has developed paradigms of great importance for the broader TOR field.
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Trends in Cell Biology,
1996]
Cellular microtubules assemble and disassemble at a variety of rates and frequencies, and these properties contribute directly to the cell-cycle-associated rearrangements of the microtubule cytoskeleton and to the molecular basis of mitosis. The kinetics of assembly/disassembly are governed, in part, by the hydrolysis of GTP bound to the B-tubulin nucleotide-binding site. The B-tubulin GTP-binding site, therefore, lies at the heart of microtubule assembly-disassembly kinetics, and the elucidation of its structure is central to an understanding of the cellular behaviour of microtubules. Unfortunately, the crystallographic structure of B-tubulin is not yet available. In this review, we describe the progress being made using mutagenesis and biochemical studies to understand the structure of this unusual GTP-binding site.
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Microbiol Mol Biol Rev,
2021]
SUMMARYExtensive use of chemical insecticides adversely affects both environment and human health. One of the most popular biological pest control alternatives is bioinsecticides based on <i>Bacillus thuringiensis</i> This entomopathogenic bacterium produces different protein types which are toxic to several insect, mite, and nematode species. Currently, insecticidal proteins belonging to the Cry and Vip3 groups are widely used to control insect pests both in formulated sprays and in transgenic crops. However, the benefits of <i>B. thuringiensis</i>-based products are threatened by insect resistance evolution. Numerous studies have highlighted that mutations in genes coding for surrogate receptors are responsible for conferring resistance to <i>B. thuringiensis</i> Nevertheless, other mechanisms may also contribute to the reduction of the effectiveness of <i>B. thuringiensis</i>-based products for managing insect pests and even to the acquisition of resistance. Here, we review the relevant literature reporting how invertebrates (mainly insects and <i>Caenorhabditis elegans</i>) respond to exposure to <i>B. thuringiensis</i> as either whole bacteria, spores, and/or its pesticidal proteins.
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[
1986]
Wild-type body wall muscle cells of Caenorhabditis elegans produce at a constant ratio two myosin heavy chain isoforms, A and B, that form homodimeric myosins. Electron microscopy of negatively stained complexes of isoform-specific antibodies with isolated thick filaments shows that the surface of the 9.7 =B5m long filament is differentiated with respect to myosin content: a medial 1.8 =B5m zone contains myosin A and two polar 4.4 = =B5m zones contain myosin B. Biochemical and electron microscopic studies show that at 0.45 M KC1, pH 6.35, myosin B and paramyosin are solubilized. The medial all-myosin A region with novel core structures extending in a polar manner remain. These dissociation experiments suggest a sequential model for wild-type thick filament assembly in which myosins A and B would participate in the initiation and termination of assembly, respectively. Analysis of mutant thick filaments clarifies the relationship of the myosin isoforms. CB190 (
unc-54 I) thick filaments contain myosin A only and have normal length. CB1214 (
unc-15 I) mutants produce no paramyosin, and their thick filaments are composed of a medial myosin region
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Results Probl Cell Differ,
2017]
Asymmetric cell division is a common mode of cell differentiation during the invariant lineage of the nematode, C. elegans. Beginning at the four-cell stage, and continuing throughout embryogenesis and larval development, mother cells are polarized by Wnt ligands, causing an asymmetric inheritance of key members of a Wnt/B-catenin signal transduction pathway termed the Wnt/B-catenin asymmetry pathway. The resulting daughter cells are distinct at birth with one daughter cell activating Wnt target gene expression via B-catenin activation of TCF, while the other daughter displays transcriptional repression of these target genes. Here, we seek to review the body of evidence underlying a unified model for Wnt-driven asymmetric cell division in C. elegans, identify global themes that occur during asymmetric cell division, as well as highlight tissue-specific variations. We also discuss outstanding questions that remain unanswered regarding this intriguing mode of asymmetric cell division.
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Exp Neurol,
2019]
Non-mammalian models of CIPN remain relatively sparse, but the knowledge gained from the few published studies suggest that these species have great potential to serve as a discovery platform for new pathways and underlying genetic mechanisms of CIPN. These models permit large-scale genetic and pharmacological screening, and they are highly suitable for in vivo imaging. CIPN phenotypes described in rodents have been confirmed in those models, and conversely, genetic players leading to axon de- and regeneration under conditions of chemotherapy treatment identified in these non-mammalian species have been validated in rodents. Given the need for non-traditional approaches with which to identify new CIPN mechanisms, these models bear a strong potential due to the conservation of basic mechanisms by which chemotherapeutic agents induce neurotoxicity.
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Trends Endocrinol Metab,
2008]
The uptake, biosynthesis and metabolism of cholesterol and other lipids are exquisitely regulated by feedback and feed-forward pathways in organisms ranging from Caenorhabditis elegans to humans. As endoplasmic reticulum (ER) membrane-embedded transcription factors that are activated in the Golgi apparatus, sterol regulatory element-binding proteins (SREBPs) are central to the intracellular surveillance of lipid catabolism and de novo biogenesis. The biosynthesis of SREBP proteins, their migration from the ER to the Golgi compartment, intra-membrane proteolysis, nuclear translocation and trans-activation potential are tightly controlled in vivo. Here we summarize recent studies elucidating the transcriptional and post-transcriptional regulation of SREBP-1c through nutrition and the action of hormones, particularly insulin, and the resulting implications for dyslipidemia of obesity, metabolic syndrome and type 2 diabetes.