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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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[
Nat Genet,
2006]
Systematic mapping of genetic interactions for Caenorhabditis elegans genes involved in signaling pathways implicated in human disease reveals a network of 350 interactions. The topology of this network resembles that mapped previously in yeast, reinforcing the idea that similar networks may underlie the genetic basis of complex human disease.
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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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Cell Host Microbe,
2009]
Similarities in innate immune signaling exist between mammals and the nematode Caenorhabditis elegans. Now, Ziegler et al. (2009) and Ren et al. (2009) demonstrate that a protein kinase C delta homolog in C. elegans is involved in innate immunity, providing evidence that the conservation of immune signaling networks extends further than previously thought.
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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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[
Mol Cell,
2014]
In this issue of Molecular Cell, Hendriks et al. (2014) uncover extensive oscillations in global gene expression during C. elegans development, in synchrony with the molting cycle.
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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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BMC Biol,
2012]
Caenorhabditis elegans is a preeminent model organism, but the natural ecology of this nematode has been elusive. A four-year survey of French orchards published in BMC Biology reveals thriving populations of C. elegans (and Caenorhabditis briggsae) in rotting fruit and plant stems. Rather than being simply a 'soil nematode', C. elegans appears to be a 'plant-rot nematode'. These studies signal a growing interest in the integrated genomics and ecology of these tractable animals.