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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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Nature,
1998]
Some species of the nematode worm (Caenorhabditis elegans) are sociable diners, clumping together to share a meal, yet others are more solitary. Why? According to a report by de Bono and Bargmann, these differences can be explained by a change of just one amino acid in a putative neuropeptide receptor.
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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,
2012]
One of the most striking properties of RNA interference (RNAi) in Caenorhabditis elegans is its persistence in offspring after the triggering double-stranded RNA (dsRNA) has disappeared. A new study reveals that a heterochromatic silencing mark is deposited around the targets of RNAi and is transmitted through generations. These results show that RNAi can induce stable and heritable chromatin modifications in animals.
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Science,
1990]
Can a lowly worm help neurobiologists untangle the pathology of Alzheimer's, Huntington's, Parkinson's, and other human brain diseases? That surprising question kept cropping up at a recent Dahlem conference on degenerative brain disorders. Although progress has been made toward understanding those disorders, conference participants had to conclude that they don't yet know nearly enough about how brain cells die. And that's where the lowly worm may
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Nat Genet,
2001]
Comparative studies of nematode development provide a powerful framework for investigating the evolution of developmental mechanisms. A recent report also demonstrates how comparative work can inform our understanding of basic developmental signaling pathways. In particular, investigation of the differences in vulva development between Caenorhabditis elegans and Pristionchus pacificus has clarified the molecular relationship between an epidermal growth factor-Ras-MAP kinase signaling pathway and downstream Hox transcription factor activity.
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[
Nature,
1994]
RNA trespasses in what was once thought to be protein's province. The notion that RNAs can be enzymes, binding specifically to ligands, cofactors and substrates, is now commonplace; yet only a few years ago, these were the sacred acts of proteins. History may be about to repeat itself. Regulatory proteins bind to specific sequences in the genes or messenger RNAs they control, and so determine how much a gene is expressed, in what cells, and when. But why should these regulators have to be protein? Why not RNA? We already know, in bacteria, of RNAs that can control gene expression through remarkably sophisticated mechanisms. Now, two reports in Cell not only identify a tiny, repressing RNA in animal cells, but also show that it acts upon a region of mRNA often thought to be barren and insignificant. Although this could be a rare, deviant case, there is the tantalizing possibility that a new family of regulatory RNAs awaits discovery.
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Nat Genet,
1992]
Predicting coding regions from genomic sequence is not entirely accurate, and predicting expression patterns of candidate genes is still a fantasy. Both of these concerns can be addressed by analysing expressed sequences (cDNA) in addition to genomic sequences. The genomic sequencing of the nematode Caenorhabditis elegans has begun; in parallel, several groups (including the genomic sequencing participants) are isolating, sequencing and mapping C. elegans cDNA clones. The first results of this endeavor, including the analysis of about 1,600 independent cDNA sequences, appear in this issue.
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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.