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[
The Journal of NIH Research,
1991]
Cowabugna, dudes! Those lean, gene-revealing machines have scored a most totally excellent victory in the battle to understand aging. We are, of course, talking about mutant ninja nematodes here. At a conference on aging in January at Cold Spring Harbor's Banbury Center, Thomas Johnson of the Institute for Behavioral Genetics at the University of Colorado in Boulder brought some dudes and dudettes from Capitol Hill up to date on the latest awesome achievements of the bodacious beasts know as Caenorhabditis elegans.
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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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[
Nature,
2000]
We thought we knew what spectrin does. Is it not the elastic, membrane-bound protein that prevents red blood cells from rupturing as they circulate in the bloodstream? And does it not have the same supporting function in other cells? The second assumption has seldom been questioned over the past two decades, but has just been overturned by the power of experimental genetics, as described in three reports in the Journal of Cell Biology. The results may bear on human diseases such as muscular dystrophy.
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[
Nature,
1998]
The human genome is predicted to contain between 50,000 and 100,000 genes. To work out what these genes do, an array of techniques is needed to evaluate the protein-protein interactions and biochemical pathways of any gene product. The nematode worm Caenorhabditis elegans is an excellent system for such studies because of its well-understood genetics and development, evolutionary conservation to human genes, small genome size and relatively short life cycle. The 100-megabase-pair genome will be completely sequenced this year, and a total of 17,000 genes have been predicted, many with human counterparts. Approaches used to manipulate gene expression in C. elegans include transposon-mediated deletion, antisense inhibition and direct isolation of deletions after mutagenesis. Although these methods have proved useful, limitations still exist.
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[
Nature,
1993]
Twenty years ago Sydney Brenner described an electrode-less plan for attacking the problems of neural development and physiology in the small nematode Caenorhabditis elegans. He proposed to set the groundwork by reconstructing the entire nervous system of the worm by serial section electron microscopy. Given the resulting wiring diagram, he thought it might be possible to make guesses as to how the nervous system worked. A second aspect of his plan was genetics: single-gene mutants exhibiting aberrant behaviour, such as uncoordinated movement, were to be analysed to address the question of how genes specify development and function of the nervous system. In two papers beginning on page 334 of this issue, McIntire et al. demonstrate that work on Brenner's plan, with a few tricks added over the years, is progressing very nicely.
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[
Nature,
1999]
Advances in human genetics have meant that the genes mutated in human diseases can be identified exclusively by their location in the genome. But how do we work out the cellular functions of the associated protein products? Reports on pages 383 and 386 of this issue begin to address this problem for two proteins - polycystin-1 (PKD1) and polycystin-2 (PKD2) - that are defective in human kidney disease. From their studies of the nematode worm Caenorhabditis elegans, Barr and Sternberg present evidence that homologues of the polycystins act together in a signal-transduction pathway in sensory neurons. Chen et al., by contrast, have used an oocyte-expression system in the from Xenopus laevis to show that a homologue of PKD2 is associated with the activity of a cation channel. These results support the hypothesis that polycystin-related proteins belong to a hitherto unknown class of signal-transduction molecules.
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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