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[
Esquire,
1985]
In the end, it is attention to detail that makes all the difference. It's the center fielder's extra two steps to the left, the salesman's memory for names, the lover's phone call, the soldier's clean weapon. It is the thing that separates the men from the boys, and, very often, the living from the dead. Professional success depends on it, regardless of the field. But in big-time genetic research, attention to detail is more than just a good work habit, more than a necessary part of the routine. In big-time genetic research, attention to detail is the very meat and the god of science. It isn't something that's expected; it is simply the way of things. Those in the field, particularly those who lead the field, are slaves to detail. They labor in submerged mines of it, and haul great loads of it up from the bottom of an unseen ocean-the invisible sea of biological phenomena, upon which all living things float. Detail's rule over genetics is total and cruel. Months and even years of work have literally gone down the drain because of the most minor miscalculations. Indeed, perhaps the greatest discovery in the history of the discipline-the double-helix structure of DNA-might have been made by Linus Pauling instead of James D. Watson and Francis H. C. Crick. But Pauling's equations contained a simple mistake in undergraduate-level chemistry, a sin against detail that is now part of the legend. Each of the six scientists singled out here has made his mark by mastering his own particular set of
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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.
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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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[
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.