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17 April 2014 12:48 pm ,
Vol. 344 ,
Officials last week revealed that the U.S. contribution to ITER could cost $3.9 billion by 2034—roughly four times the...
An experimental hepatitis B drug that looked safe in animal trials tragically killed five of 15 patients in 1993. Now,...
Using the two high-quality genomes that exist for Neandertals and Denisovans, researchers find clues to gene activity...
A new report from the Intergovernmental Panel on Climate Change (IPCC) concludes that humanity has done little to slow...
Astronomers have discovered an Earth-sized planet in the habitable zone of a red dwarf—a star cooler than the sun—500...
Three years ago, Jennifer Francis of Rutgers University proposed that a warming Arctic was altering the behavior of the...
- 17 April 2014 12:48 pm , Vol. 344 , #6181
- About Us
Growing Old Together
6 April 2001 7:00 pm
Three new studies suggest that creatures as different as worms, flies, and yeast in fact break down in similar ways as they pass their primes. Scientists speculate that the parallels will transfer to mammals, as well.
The molecular details of aging are best known in the roundworm Caenorhabditis elegans. A molecular signaling pathway determines the worm's life-span. At the heart of the pathway lies the daf-2 gene, which encodes a member of the insulin family of cell surface receptors. Certain mutations in daf-2 allow worms to wriggle into ripe old ages that greatly exceed those of their normal counterparts. Scientists have succeeded in fleshing out many details of the process, but there was no particular reason to think that other species would control aging with the same pathway.
Now, two teams report in the 6 April issue of Science that a related insulin-like pathway shapes life-span in fruit flies as well. Females that carry only defective copies of the daf-2 equivalent (InR) buzz around long after normal flies keel over, according to a group led by Marc Tatar, an evolutionary geneticist at Brown University in Providence, Rhode Island. Similarly, animals with inactive versions of another member of the pathway called chico flit into extreme dotage, report geneticists Linda Partridge and David Gems of University College London and colleagues.
Even yeast have some similarities. In a third study published online by Science on 6 April (www.sciencexpress.org), molecular geneticist Valter Longo of the University of Southern California in Los Angeles and colleagues battered a population of yeast mutants with heat or paraquat, a chemical that creates reactive oxygen molecules. Among the survivors, they found two strains that lived longer than wild-type yeast. One of the mutants carries a defect in Sch9, which resembles two genes in the C. elegans daf-2 pathway. When the researchers engineered a deletion of Sch9, they found that the resulting strain survived three times longer than did wild-type cells.
"It's all coming together," says molecular geneticist Cynthia Kenyon of the University of California, San Francisco. "This aging system that we know about in the worm is out there in other animals, regulating their aging. Maybe not in the same exact form, but it's there. It's unbelievable, simply unbelievable."