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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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[
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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[
Nat Neurosci,
2003]
In C. elegans, social and solitary feeding behavior can be determined by a single amino acid change in a G protein-coupled receptor. A new study identifies ligands for this receptor and suggests how changes in behavior evolve at the molecular level.
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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.
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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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[
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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[
Trends Endocrinol Metab,
2001]
In Caenorhabditis elegans, an insulin-like signalling pathway culminates in a transcription factor (TF) that is homologous to a subfamily of Tps responsible for the regulation of a subset of insulin-responsive genes in humans. Under harsh conditions, C. elegans reduces signalling through this pathway and arrests developmentally in a manner that is similar to the metabolic syndrome of humans. We propose that an understanding of this pathway could lead to drugs with optimal potency and selectivity in the treatment of type 2 diabetes mellitus.
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[
Science,
2002]
The nematode worm known as Caenorhabditis elegans is not much to look at. Just a millimeter long and transparent to boot, it is almost invisible to the naked eye. But in biological research the tiny worm looms large, providing a model system for studying everything from embryonic development to aging. Now, three researchers who pioneered the use of C. elegans as a model organism have won the Nobel Prize in Physiology or Medicine.
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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,
1990]
An exhaustive study of the tiny roundworm C. elegans has revealed a wealth of information about development and the brain. And now the effort to decipher the worm's genome is fast becoming the benchmark by which the human genome project will be measured.