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[
New York Times,
1991]
Through a microscope, they look like tiny crystal serpents, curving and slithering across the dish with an almost opiated languor, doubling back on themselves as though discovering their tails for the first time, or bumping up against a neighbor clumsily and then slowly recoiling. Beneath their translucent skin the pulsing muscle cells and nerve fibers are clearly visible, a sight so strange and so exquisite that it is hard to believe these creatures are common roundworms, found in gardens and compost heaps everywhere. And it is harder still to believe that such slippery squiggles of life are fast changing the face of fundamental biology.
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[
Experimental Neurology,
1975]
The precision of neuronal development is programmed genetically. The genes involved must be expressed in an orderly sequence so that their products appear in the right cell at the right time. By studying mutants in which this sequence is altered, it should be possible to dissect the development and recognize the steps controlled by individual genes.
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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,
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.
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[
Science,
1996]
The one-cell animal embryo, or zygote, faces a daunting engineering task: implementing the architectural plans inscribed in its DNS for building a complex, multicelled body. So, like any sensible construction supervisor, the zygote swiftly divides the project into manageable chunks, assigning some of its progeny to build only gut, for example, and other to make only muscle or skin. Just how each early embryonic cell gets its orders is understood only for the fruit fly Drosophila melanogaster-an achievement that helped win 1995's Nobel Prize in medicine for three developmental biologists. Now, however, the communication lines governing embryonic development are emerging in another animal beloved of developmental researchers: the tiny worm known as Caenorhabditis elegans.
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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.