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J Neurobiol,
1993]
Mutations causing a touch-insensitive phenotype in the nematode Caenorhabditis elegans have been the basis of studies on the specification of neuronal cell fate, inherited neurodegeneration, and the molecular nature of mechanosensory transduction. (C) 1993 John Wiley & sons, Inc.
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Human Genome News,
1999]
For the first time, scientists have the nearly complete genetic instructions for an animal that, like humans, has a nervous system, digests food, and reproduces sexually. The 97-million-base genome of the tiny roundworm Caenorhabditis elegans was deciphered by an international team led by Robert Waterston and John Sulston. The work was reported in a special issue of the journal Science (December 11, 1998) that featured six articles describing the history and significance of the accomplishment and some early sequence-analysis results.
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Science,
1994]
In 1967, Sydney Brenner isolated the first behavioral mutants of the nematode Caenorhabditis elegans, and in 1970, John White began the systematic reconstruction of its nervous system. This dual approach of genetics coupled with detailed morphological analysis, now enhanced by the tools of molecular biology and electrophysiology, still dominates the study of the function and development of the C. elegans nervous system. Although Brenner's vision of a comprehensive understanding of this simple animal has taken time to mature, findings of the past few years indicate that the tree is bearing fruit.
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Parasitol Today,
1990]
Many aspects of the biology of kinetoplastids are unique, so it is surprising that they share with nematodes an unusual post-transcriptional process called trans-splicing. During this process, a small conserved RNA sequence is added to the 5' non-translated ends of transcribed RNAs of protein-encoding genes. Trypanosomes and nematodes are the only organisms to date in which these sequences have been described, and the biological significance of trans-splicing remains a mystery but may be of wider occurrence in invertebrates. In this review, John Donelson and Wenlin Zeng compare the process in nematodes and trypanosomes and speculate on its raison d'etre.
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J Pathol,
2009]
Virtually every tissue of the adult organism maintains a population of putatively slowly-cycling stem cells that maintain homeostasis of the tissue and respond to injury when challenged. These cells are regulated and supported by the surrounding microenvironment, referred to as the stem cell ''niche''. The niche includes all cellular and non-cellular components that interact in order to control the adult stem cell, and these interactions can often be broken down into one of two major mechanistic categories-physical contact and diffusible factors. The niche has been studied directly and indirectly in a number of adult stem cell systems. Herein, we will first focus on the most well-understood niches supporting the germline stem cells in the lower organisms Caenorhabditis elegans and Drosophila melanogaster before concentrating on the more complex, less well-understood mammalian niches supporting the neural, epidermal, haematopoietic and intestinal stem cells. Copyright (c) 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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Studies of History & Philosophy of Science,
1998]
In 1963, just a year after the researchers of the Medical Research Council (MRC) Unit of Molecular Biology in Cambridge, joined by some other research groups, has moved from various scattered and makeshift buildings in the courtyard of the Physics Department to a lavishly funded four-storey laboratory, B. Lush, the Principal Medical Officer of the MRC, came to inquire about their plans for future expansion. He indicated that the MRC wished to build the laboratory up to what the principal researchers considered its 'final size' until their retirement, which meant planning ahead for at least 15 years. This surprising move was doubtless prompted by the recent award of the Nobel Prize to three members of the laboratory, Max Perutz, John Kendrew and Francis Crick, for their work on the molecular structure of proteins and nucleic acids. The triple award had propelled the new Laboratory of Molecular Biology into the limelight, and the MRC was interested in securing optimal research conditions for this prestigious group of researchers.
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Science,
2004]
I'm one of the 2000 or so worm people who study the tiny nematode Caenorhabditis elegans. When we are asked by an outsider why we play with worms, our much-practiced answer goes something like this: In the
mid-1960s, Sydney Brenner chose C. elegans as a model organism for elucidating animal development and behavior because of the roundworm's cellular simplicity and advantages for genetic studies. The analysis of mutants helps us learn what the nonmutant versions of genes do. We know the location and lineage of every cell in an adult C. elegans as well as the wiring of all the worm's 302 neurons, down to the last synapse. C. elegans was the first multicellular organism to have its DNA completely sequenced (1), and many of its genes resemble those of humans and do similar jobs. The importance of such research was highlighted when Brenner, John Sulston, and Bob Horvitz were awarded the 2002 Nobel Prize in physiology or medicine for their worm work.
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Cell Death Differ,
2004]
Awarding the 2002 Nobel Prize in Physiology or Medicine to Sydney Brenner, H Robert Horvitz, and John E Sulston for 'their discoveries concerning the genetic regulation of organ development and programmed cell death (PCD)' highlights the significant contribution that the study of experimental organisms, such as the nematode Caenorhabditis elegans, has made to our understanding of human physiology and pathophysiology. Their studies of lineage determination in worms established the 'central dogma' of apoptosis: The BH3-only protein EGL-1 is induced in cells destined to die, interacts with the BCL-2-like inhibitor CED-9, displacing the adaptor CED-4, which then promotes activation of the caspase CED-3. The vast majority of cells undergoing PCD during development in C. elegans, as in vertebrates, are neurons. Accordingly, the genetic regulation of apoptosis is strikingly similar in nematode and vertebrate neurons. This review summarizes these similarities - and the important differences - in the molecular mechanisms responsible for neuronal PCD in C. elegans and vertebrates, and examines the implications that our understanding of physiological neuronal apoptosis may have for the diagnosis and treatment of acute and chronic human neurodegenerative
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J Appl Toxicol,
2016]
Caenorhabditis elegans is a small nematode that can be maintained at low cost and handled using standard in vitro techniques. Unlike toxicity testing using cell cultures, C. elegans toxicity assays provide data from a whole animal with intact and metabolically active digestive, reproductive, endocrine, sensory and neuromuscular systems. Toxicity ranking screens in C. elegans have repeatedly been shown to be as predictive of rat LD50 ranking as mouse LD50 ranking. Additionally, many instances of conservation of mode of toxic action have been noted between C. elegans and mammals. These consistent correlations make the case for inclusion of C. elegans assays in early safety testing and as one component in tiered or integrated toxicity testing strategies, but do not indicate that nematodes alone can replace data from mammals for hazard evaluation. As with cell cultures, good C. elegans culture practice (GCeCP) is essential for reliable results. This article reviews C. elegans use in various toxicity assays, the C. elegans model's strengths and limitations for use in predictive toxicology, and GCeCP. Published 2016. This article is a U.S. Government work and is in the public domain in the USA. Journal of Applied Toxicology published by John Wiley & Sons Ltd.
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Parasitol Today,
1992]
Like particle physics, biology is now a big expensive business, and like CERN, the genome projects alternately provoke admiration and detraction. Some feel that it would be more valuable to go for specific genes of interest rather than fill databases with sequences of junk DNA. The detractors would also say that the costs entailed, the limited intellectual and practical payback, and the ethical worries are too big to justify. But like the mythological juggernaut, once started it won't stop and it is indisputable that exciting information will come out of these efforts. Like some of the best discoveries many will be unexpected and have repercussions of immense value. This is indisputable on statistical grounds alone; the Caenorhabditis elegans genome is estimated to contain tens of thousands of genes. However, genome projects cannot be justified by serendipity and they do have obvious immediate value for tracing the genes involved in cancer and other inheritable disorders, and indeed for the multiple technological spin-offs. The C. elegans genome project is already bearing luscious fruit, of the 34 genes reported so far some of which have sequence similarity with genes such as glutathione reductase, an immunogenic protein from Trichostrongylus colubriformis, acetyl-CoA acetyltransferase and various other enzymes, growth factors and signal transducing components. Up-to-date cDNA data will be published by John Sulston and his colleagues in the early issues of Nature Genetics, due out this month.