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Science,
1984]
The end of 1983 saw the completion of a major project in developmental biology. All the cell divisions, deaths, and migrations that generate the embryonic, then the larval, and finally the adult forms of the roundworm Caenorhabditis elegans have now been traced. It is the first time the complete cell lineage of an organism of this degree of complexity, one that contains many of the diverse cell types found in all higher animals, has been determined.
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[
Discover,
1991]
Undulating under the microscope, its muscle and nerve cells visible within its transparent body, the tiny roundworm Caenorhabditis elegans is normally a creature of surprising grace. But one mutant strain is not elegans at all. It thrashes about in such an uncoordinated fashion that researchers have dubbed the mutant worm "unc"...
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Nat Genet,
2003]
A new study attempts to amplify and clone all the predicted protein-encoding open reading frames (ORFs) for Caenorhabditis elegans. This analysis confirms many of the predicted genes but suggests roughly 50% of them require correction. Recombining the ORFs into a number of different expression systems can generate functional proteomics kits for characterizing protein activity and interaction networks.
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Nature,
1999]
Life is based on social contract, genes work for the good of the organism, and they are reproduced. But certain rogue genes, called transposons, wantonly reproduce at the expense of the organism, inserting new copies of themselves all over the genome. Reporting in Cell, Tabara et al., and Ketting et al. now show that organisms have systems to hold transposons in check. They suggest that one of the clues that organisms use to detect illicit activity is double-stranded RNA, and their results could explain the reason for the mysterious phenomenon of RNA interference.
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Science,
1996]
What 's the secret to long life? For the nematode Caenorhabditis elegans, it's slow, easy living, in which all life's events occur in a leisurely rhythm, according to work described on page 1010 of this issue. The new research, by Siegfried Hekimi and Bernard Lakowski of McGill University in Montreal, identifies four genes that, when mutated, can make these worms use energy more efficiently, feed and swim at a slower pace-and live many times their normal life-span. Some of the experimental nematodes lived for almost 2 months, far longer than their expected 9 days.
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Nature,
1996]
During the development of many, if not all, complex organisms, specific cells are marked out for elimination in a process known as programmed cell death, or apoptosis, a form of cell suicide. For example, during the development of the hermaphrodite nematode worm Caenorhabditis elegans, 131 of the 1,090 cells produced are genetically destined to die. Drosophila embryos without the necessary genes to execute this death programme do not survive. In vertebrates, failure to delete malformed or potentially autoreactive immune cells during development can eventually lead to autoimmunity or leukaemia. So too much or too little cell death threatens the whole organism.
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Nature,
1999]
Animal evolution is commonly viewed as producing diverse, environmentally adapted bodies to propagate the germ line. The evolutionary theory of ageing suggests that genetic limits to lifespan may be inadvertent consequences of evolutionary selection for maximizing that propagation. In other words, trade-offs occur that favour reproductive success over post-reproductive longevity; lifespan should be inversely correlated with fecundity when progeny production diverts resources from the maintenance of somatic (non-reproductive) cells. The germ line contains all the genetic information to specify the soma. But it is also possible that there are other, environmentally modulated instructions for life history that the germ line conveys to the soma to maximize reproduction.
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Nature,
1998]
In 1983, John Sulston and Alan Coulson began to construct a complete physical map of the genome of the nematode worm Caenorhabditis elegans, and started what became known as the C. elegans Genome Project. At the time, several people wondered why John, who had just described all of the cell divisions in C. elegans (the cell lineage), was interested in this project rather than in a more 'biological' problem. He replied by joking that he had a "weakness for grandiose, meaningless projects". In 1989, as the physical map approached completion, the Genome Project, now including Bob Waterston and his group, embarked on the even more ambitious goal of obtaining the complete genomic sequence
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Science,
1984]
In a dimly lit laboratory room in Gottingen, West Germany, Einhard Schierenberg bent his long, angular frame over his microscope, watching and counting, recording what he saw on charts and videotapes, hour upon hour, day after day, intermittently for six years. Five hundred miles away in a tiny, starkly equipped cubbyhole in Cambridge, England, John Sulston was doing the same thing, hunched over his microscope, earphones on his head to block any sound that might divert him from the image in his eyepiece. Sometimes he would sit watching all day long, diligently marking in a notebook with his colored pens. Schierenberg and Sulston were learning, cell by cell, how to build a worm.
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Science,
1996]
Geoffrey Gold, a physiologist at the Monell Chemical Senses Center in Philadelphia, had wanted for years to put to rest a nagging question: How do odors trigger olfactory neurons to fire off action potentials to the brain? The dogma for the past 5 years had been that odors fall into two catagories, each of which acts via a different inracellular messenger molecule. But Gold believed this view was wrong, and that all odors work by increasing the production of the intracellular messenger cyclic AMP (cAMP). One day last spring, Gold got a phone call out of the blue from neurobiologist John Ngai, at the University of California (UC), Berkeley, offering the possibility of answering this question. It was my dream come true," says Gold. ......