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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 Mol Biol,
2015]
Maf1 was first identified in yeast, and studies in metazoans have primarily focused on examining its role in the repression of transcription that is dependent on RNA polymerase III. Recent work has revealed a novel and conserved function for Maf1 in the maintenance of intracellular lipid pools in Caenorhabditis elegans, mice, and cancer cell lines. Although additional Maf1 targets are likely, they have not been identified, and these recent findings begin to define specific activities for Maf1 in multicellular organisms beyond the regulation of RNA polymerase III transcription and suggest that Maf1 plays a more diverse role in organismal physiology. We will discuss these newly defined physiological roles of Maf1 that point to its placement as an important new player in lipid metabolism with implications in human metabolic diseases such as obesity and cancer, which display prominent defects in lipid homeostasis.
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Cell,
2001]
In 1998, The C. elegans Sequencing Consortium (1998) announced the essentially complete Caenorhabditis elegans genomic sequence, setting a high standard for sequencing multicellular genomes. As of April 2001, the C. elegans genome, including repetitive regions, is >99.6% complete with sequence equivalent to what many genome projects call phase III. How has this changed the lives of C. elegans researchers, and our view of the worm?
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Seminars in Developmental Biology,
1992]
At the 4-cell stage of the C. elegans embryo, three axes can be defined: anterior-posterior (A-P), dorsal-ventral (D-V), and left-right (L-R). The A-P axis first becomes obvious in the newly fertilized 1-cell embryo. Pronouned cytoplasmic assymmetries arise along the A-P axis during the first cell cycle, after which the zygote undergoes a series of stem cell-like cleavages with an A-P orientation of the mitotic spindle; these cleavages generate several somatic founder cells and a primordial germ cell. The D-V and L-R axes are defined by the direction of spindle rotation as the 2-cell embryo divides into four cells. In contrast to the A-P axis, there do not appear to be cellular asymmetries associated with the D-V and L-R axes, and both axes can easily be reversed by micromanipulation. Thus, with respect to the roles that the embryonic axes serve in cell-fate determination in the early C. elegans embryo, it appears that internally transmitted developmental information is differentially segregated along the A-P axis, but not along the D-V or L-R axes. Instead, D-V and L-R differences in the fates of cells within lineages appear to be dictated by differential
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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.