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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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Trends Genet,
1997]
The 100 Mb sequence of the nematode Caenorhabditis elegans genome will be completed in 1998. More than 10,000 predicted genes have been identified to date, so it should come as no surprise to find a C. elegans homologue of your favourite gene in current databases. For some investigators, the discovery of a C. elegans homologue represents a unique opportunity to adopt a genetic approach and to take advantage of the extensive repertoire of C. elegans gene characterization and manipulation tools. RNA injection provides a quick and efficient method for obtaining clues about wild-type gene function. Reverse genetic approaches also make it feasible to screen de novo for mutations in specific gene sequences. This review highlights the resources available for analysing a C. elegans homologue, starting from the gene sequence and proceeding to the biological function.
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Lipids,
1991]
Parasitic nematodes do not biosynthesize sterols de novo and therefore possess a nutritional requirement for sterol, which must be obtained from their hosts. Consequently, the metabolism of phytosterols by plant-parasitic nematodes is an important process with potential for selective exploitation. The sterol compositions of several species of plant-parasitic nematodes were determined by capillary gas chromatography-mass spectrometry and compared with the sterol compositions of their hosts. Saturation of the phytosterol nucleus was the major metabolic transformation performed by the root-knot nematodes Meloidogyne arenaria and M. incognita and the corn root lesion nematode, Pratylenchus agilis. In addition to saturation, the corn cyst nematode, Heterodera zeae, dealkylated its host sterols at C-24. Because free-living nematodes can be cultured in sterol-defined artificial medium, they have been successfully used as model organisms for investigation of sterol metabolism in plant-parasitic nematodes. Major pathways of phytosterol metabolism in Caenorhabditis elegans, Turbatrix aceti and Panagrellus redivivus included C-24 dealkylation and 4 alpha-methylation (a pathway unique to nematodes). C. elegans and T. aceti introduced double bonds at C-7, and T. aceti and P. redivivus saturated the sterol nucleus similarly to the plant-parasitic species examined. Several azasteroids and long-chain dimethylalkylamines inhibited growth and development of C. elegans and also the delta 24-sterol reductase enzyme system involved in the nematode C-24 dealkylation pathway.
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Cell,
1998]
Since the rise of the field of sociobiology, the study of the biological basis of social behavior, scientists have striven to assign genetic origins for a variety of social behaviors. There have been a number of highly publicized and often controversial studies of the basis of human social behavoirs such as sexual orientation and religion. Less trumpeted by the popular press, there have been a number of more credible advances in the genetic analysis of complex behavioral traits. Two papers in the past year, one in this issue of Cell (de Bono and Bargmann, 1998), have established two interesting cases of a molecular basis for complex behaviors that are arguably relevant to social interactions in natural populations. Both have to do with food foraging strategies, one in Drosophila and one in C.
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Traffic,
2013]
The germline and embryo of the nematode Caenorhabditis elegans have emerged as powerful model systems to study membrane dynamics in an intact, developing animal. In large part, this is due to the architecture of the reproductive system, which necessitates de novo membrane and organelle biogenesis within the stem cell niche to drive compartmentalization throughout the gonad syncytium. Additionally, membrane reorganization events during oocyte maturation and fertilization have been demonstrated to be highly stereotypic, facilitating the development of quantitative assays to measure the impact of perturbations on protein transport. This review will focus on regulatory mechanisms that govern protein trafficking, which have been elucidated using a combination of C. elegans genetics, biochemistry and high-resolution microscopy. Collectively, studies using the simple worm highlight an important niche that the organism holds to define new pathways that regulate vesicle transport, many of which appear to be absent in unicellular systems but remain highly conserved in mammals.
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J Cell Biochem,
2013]
microRNA (miRNA) is a family of small, non-coding RNA first discovered as an important regulator of development in Caenorhabditis elegans (C. elegans). Numerous miRNAs have been found in C. elegans, and some of them are well conserved in many organisms. Though, the biologic function of miRNAs in C. elegans was largely unknown, more and more studies support the idea that miRNA is an important molecular for C. elegans. In this review, we revisit the research progress of miRNAs in C. elegans related with development, aging, cancer, and neurodegenerative diseases and compared the function of miRNAs between C. elegans and human.
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Methods Mol Biol,
2006]
The genome of the nematode Caenorhabditis elegans was the first animal genome sequenced. Subsequent sequencing of the Caenorhabditis briggsae genome enabled a comparison of the genomes of two nematode species. In this chapter, we describe the methods that we used to compare the C. elegans genome to that of C. briggsae. We discuss how these methods could be developed to compare the C. elegans and C. briggsae genomes to those of Caenorhabditis remanei, C. n. sp. represented by strains PB2801 and CB5161, among others (1), and Caenorhabditis japonica, which are currently being sequenced.
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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.