From the announcement:
This year's Nobel Prize in Physiology or Medicine is awarded to three scientists who have solved a major problem in biology: how the chromosomes can be copied in a complete way during cell divisions and how they are protected against degradation. The Nobel Laureates have shown that the solution is to be found in the ends of the chromosomes – the telomeres – and in an enzyme that forms them – telomerase.
A normal human cell has 46 chromosomes - the strings of all of our DNA, the code that makes us who we are. DNA is made of 4 different nucleotides - A, C, T, and G. The order in which these letters appear encode proteins within the DNA. Not all DNA encodes for a protein. Some has the role in regulation of the genes. Elizabeth Blackburn and Jack Szostak discovered that the ends of chromosomes contain a repeating sequence that is typically enriched for the base G.
When cells divide and the DNA is replicated to make the daughter cells the DNA on the ends of the chromosomes cannot be completely duplicated because of the asymmetric way in which DNA is copied. For this reason, having a gene at the end of a chromosome would be a very bad thing since it would not be passed along in the correct form to the daughter cells. In this way, having the repeating telomere sequence at these ends protects the cell from defects.
However, this incomplete replication of the end sequences also applies to the telomere and so the ends of chromosomes can be shortened with each cycle of cell division. So, the length of telomere sequences can be an indication of aging. As the telomere sequence gets shorter and shorter, a series of events called programmed cell death is triggered which rids the organism of that particular cell with the potentially damaged chromosomes. Carol Greider and Elizabeth Blackburn identified an RNA-protein complex called telomerase which can add telomere sequences to the ends of chromosomes. The activity of this complex overcomes the incomplete replication of the telomere sequence.
Now, you may notice there's a potential trouble here. If one is able to keep the chromosomes from shortening by maintaining the telomere sequence, then you might have the potential to slow the aging process. In fact, this has been shown in the model organism C. elegans. However, if a particular cell had a particularly active telomerase and was able to keep it's chromosome ends sufficiently long, then that cell might begin to behave as immortal - a pathway that might lead to cancer. In fact, telomerase has been a target for both anti-aging as well as chemotherapeutic agents.
Congratulations to Drs. Blackburn, Greider, and Szostak.