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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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Nat Methods,
2006]
RNA interference (RNAi) and automated high-throughput screening is a promising combination. But the first systematic large-scale mapping of genetic interactions in an animal shows that manual methods still have advantages over sophisticated automated screens.
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Nat Genet,
2009]
The global patterning of histone lysine methylation has been scrutinized over the years in an effort to uncover unique features indicative of chromatin function. A study in Caenorhabditis elegans now shows that nucleosomes covering exons and introns on active genes are differentially marked by H3K36 trimethylation, suggesting a new mode of communication between chromatin and pre-mRNA processing.
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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.
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Nature,
1999]
Once, lifespan genetics was largely the domain of theorists, who tried to explain why an organism's genes so cavalierly allow individual somas to die. But a flood of papers on the nematode worm Caenorhabditis elegans has brought the subject into the realm of serious experimental analysis. The latest studies (1,2), including a report by Apfeld and Kenyon (1) on page 804 of this issue, indicate that the nervous system has a key function in regulating lifespan. Perhaps we are, indeed, only as old as we think
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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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Nat Cell Biol,
2011]
Aurora A kinase is a key regulator of cell division, whose functions were attributed to its ability to phosphorylate diverse substrates. Aurora A is now shown to have a kinase-independent role in the regulation of chromatin-mediated microtubule assembly.
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[
Discover,
1991]
Undulating under the microscope, its muscle and nerve cells visible within its transparent body, the tiny roundworm Caenorhabditis elegans is normally a creature of surprising grace. But one mutant strain is not elegans at all. It thrashes about in such an uncoordinated fashion that researchers have dubbed the mutant worm "unc"...
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[
Science,
1995]
The contrasts between the sexes have inspired countless plays, novels, and other creative works. Sex differences inspire a group of developmental biologists, too-but there's a twist. While artists and most of the rest of us are fascinated by the effects of the male-female divide, these biologists are trying to learn how it arises in the first place. Their goal: to trace out the gene pathways that turn an embryo into a male or female. This quest has recently become one of the hottest areas of developmental biology, as two meetings held this year and devoted solely to the subject attest.
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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.