An enzyme that keeps cells young has won a bit of immortality for the scientists who discovered it. This year's Nobel Prize in physiology or medicine recognizes Elizabeth Blackburn of the University of California, San Francisco; Carol Greider of Johns Hopkins University School of Medicine in Baltimore, Maryland; and Jack Szostak of Harvard Medical School in Boston, each of whom receive one-third of the $1.4 million prize, for their work describing telomeres and telomerase. The trio has long been considered top contenders for the prize. "I've been hoping for this for about 10 years. I'm thrilled," says Titia de Lange of Rockefeller University in New York City, who studies telomeres.
Telomeres are repetitive stretches of DNA that cap the ends of chromosomes. First described in the 1950s, telomeres were initially thought to prevent chromosomes from attaching to each other. In 1982, Blackburn and Szostak showed that the telomere sequence from a single-celled organism called a tetrahymena could prevent the usual degradation of foreign DNA that was inserted into yeast, suggesting that telomeres work to protect DNA. It has later became clear that telomeres also help their own cell's DNA: DNA-copying enzymes can't read all the way to the end of the chromosome, inevitably producing a slightly shorter copy than the original; without telomeres, important stretches of DNA would be lost every time a cell divides.
Two years later, while Greider was a graduate student in Blackburn's lab, she discovered the enzyme telomerase, which adds telomere sequences to the ends of chromosomes, keeping them "topped up" and long enough to make up for the shortening during cell division. The pair isolated and characterized the enzyme, which is part protein and part RNA. (The RNA provides a template for the telomere DNA sequence.)
Work from Szostak's lab and Blackburn's lab showed that without telomerase, cells will eventually stop dividing and will die. Some people initially guessed that telomerase might be a fountain of youth, preventing aging in both cells and entire organisms. But the story isn't that simple. Many types of cancer cells, it turns out, have overactive telomerase that allows them to continue dividing when they shouldn't. There are clinical trials under way testing whether a vaccine against telomerase could help fight certain kinds of cancer.
Not having enough telomerase is bad news as well, though. A rare disorder called dyskeratosis congenita, which causes symptoms that resemble premature aging, is caused by a faulty telomere-maintenance system. That discovery hasn't yet led to a treatment for the disease, says Tom Vulliamy of the University of London, who studies the disorder. "Sometimes we're a bit impatient in how quickly our discoveries impact in health care. ... I am sure that the understanding of telomeres will help us treat patients someday."
This year's prize is the first Nobel to be shared by two women. Blackburn and Greider are just the ninth and 10th women, respectively, to be awarded the prize in physiology or medicine in the award's 108-year history.
For full coverage of this prize, see the 9 October issue of Science.