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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. ......
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[
Nature,
1998]
Cytochrome c leads a double life. When a cell is called on to commit apoptotic suicide, cytochrome c relocalizes from the mitochondria to the cytosol. There, it helps to activate the foot-soldiers of apoptosis - the death proteases known as caspases. How cytochrome c escapes from the mitochondria is still a matter of debate, but it is clear that certain elements within the apoptotic regulatory hierarchy do not condone such behavior. In particular, overexpression of the cell-death suppressors Bcl-2 and Bcl-xL prevents the release of cytochrome c, suggesting that these proteins act upstream of cytochrome c in the pathway to death. However, on pages 449 and 496 of this issue, Zhivotovsky et al. and Rosse et al. show that Bcl-2 can also protect cells downstream of cytochrome c release, forcing a re-evaluation of this newly acquired dogma.
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[
Science,
1998]
The near completion of the sequence of the C. elegans genome should provide researchers with a gold mine of information on topics ranging from evolution to gene
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[
Nature,
2003]
The genome of the microscopic worm Caenorhabditis briggsae has been sequenced, and show some remarkable differences from the genome of the better known - and physically similar - C. elegans.
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[
BMB Rep,
2018]
Mitochondria are crucial organelles that generate cellular energy and metabolites. Recent studies indicate that mitochondria also regulate immunity. In this review, we discuss key roles of mitochondria in immunity against pathogen infection and underlying mechanisms, focusing on discoveries using Caenorhabditis elegans. Various mitochondrial processes, including mitochondrial surveillance mechanisms, mitochondrial unfolded protein response (UPRmt), mitophagy, and reactive oxygen species (ROS) production, contribute to immune responses and resistance of C. elegans against pathogens. Biological processes of C. elegans are usually conserved across phyla. Thus, understanding the mechanisms of mitochondria-mediated defense responses in C. elegans may provide insights into similar mechanisms in complex organisms, including mammals.
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[
Nat Neurosci,
2001]
A characterization of C. elegans lacking the gene for Rim suggests that this protein may be involved in pruning synaptic vesicles for fusion, not in docking or organizing active zones.
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[
Science,
1997]
A gene that helps control the life-span of the nematode C. elegans encodes the worm version of the insulin receptor, thereby providing a possible link between aging and glucose metabolism.
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[
Nat Neurosci,
2003]
A new study in this issue demonstrates that two GABAergic motor neurons in C. elegans are excitatory at target muscles because GABA activates a ligand-gated cation conductance, which is structurally similar to several other ligand-gated channels.