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Patricia Van Arnum was executive editor of Pharmaceutical Technology.
The 2009 Nobel Prize in Physiology or Medicine was awarded to three US researchers for the discovery of how chromosomes are protected from degradation by telomeres and the enzyme telomerase during cell division.
The 2009 Nobel Prize in Physiology or Medicine was awarded to three US researchers for the discovery of how chromosomes are protected from degradation by telomeres and the enzyme telomerase during cell division. The award recognizes the researchers’ contribution in adding a new dimension to the understanding of the cell, shedding light on disease mechanisms, and for stimulating the development of potential new therapies.
The award went to Elizabeth H. Blackburn, a professor of biology and physiology at the University of California, San Francisco; Carol W. Greider, a professor of molecular biology and genetics at the John Hopkins University School of Medicine; and Jack Szostak, professor of genetics at Harvard Medical School, investigator in the department of molecular biology at Massachusetts General Hospital, and investigator at the Howard Hughes Medical Institute.
The researchers were recognized for solving a major problem in biology: how chromosomes can be copied in a complete way during cell divisions and how they are protected against degradation. Their work showed that the solution is in the ends of the chromosomes-the telomeres-and in an enzyme that forms them, telomerase, according to a press release from the Nobel Foundation.
Long, thread-like DNA molecules that carry genes are packed into chromosomes; the telomeres are the caps on their ends. Blackburn and Szostak discovered that a unique DNA sequence in the telomeres protects the chromosomes from degradation, according to the release.
Greider and Blackburn identified telomerase, the enzyme that makes telomere DNA. These discoveries explained how the ends of the chromosomes are protected by the telomeres and that they are built by telomerase. If the telomeres are shortened, cells age. Conversely, if telomerase activity is high, telomere length is maintained, and cellular senescence is delayed. This is the case in cancer cells. Certain inherited diseases, in contrast, are characterized by a defective telomerase, resulting in damaged cells. “The award of the Nobel Prize recognizes the discovery of a fundamental mechanism in the cell, a discovery that has stimulated the development of new therapeutic strategies,” according to the release.
The researchers will be awarded the Nobel Prize in a ceremony in Stockholm on Dec. 10, 2009.