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Telomeres 86

A story about shoestrings which revolutionized the world of science.

October 5th, 2009, San Francisco, early morning. Elizabeth Blackburn is still sleeping. Suddenly the phone rings and wakes her up. What she is about to learn will change her life; she and her two colleagues have just been awarded the Nobel Prize for Medicine, for their work on telomeres and telomerase. The life work of this Hobart native–(a small town on the island of Tasmania, Australia), now a molecular biology professor at UCSF, has just received its ultimate recognition.

All of this began in 1961 when a researcher at the University of Philadelphia, Leonard Hayflick, discovered that our cells eventually lose their ability to reproduce themselves. He noticed that after about 50 to 70 divisions, the cell loses the ability to regenerate itself and enters a state which scientists dub ‘cellular senescence’. But Hayflick also observed that the cells’ ability to duplicate was also influenced by the individual’s age. The cells of a young, 30-year-old man multiplied more rapidly than those of a 60-year-old man, and his cells multiplied faster than those of a 90-year-old! What Hayflick discovered was a sort of inescapable clock mechanism present in all of our cells. This countdown was probably the product of accumulated cell damage, especially in our DNA; there was therefore something very specific in our cells which made us age and limited our longevity, but Hayflick did not yet know what.

This DNA loss with every duplication is a disaster for our life-sustaining proteins, and if this occurred regularly, we would all die after 70 divisions! But since this isn’t the case, something else must be going on which stifles this process of programmed death.

Alekseï Olovnikov, a Russian biologist, was one of the first to describe telomeres in 1973. Telomeres, from the Greek word stelos (end) and meros (part), are a structure capping the extremities of the chromosomes’ DNA strands, rather like the crimps on the end of a shoelace. These DNA sequences, resembling something like TTAGGG, are repeated hundreds of times, which means that even if, during every division, some DNA is lost at the end of the telomere, it has no immediate effect on the DNA’s effectiveness, since the same sequence is found just before it, and before that one as well… until we run out of these sequences. This is when cellular senescence, and aging, begin.

Today we can measure telomere length. This is so simple nowadays that some labs in the United States and in Spain even offer this service to the general public. DNA and telomeres are organized into units, called nucleotides. These units are lined up like beads on a string, and their number can be assessed thanks to these specific tests. This is how we know that at the moment of conception, the embryo has telomeres 15,000 nucleotides long, and that at birth, telomeres have already shrunk down to 10,000 nucleotides. These telomeres continue to shorten with time, and when their length is of no more than 5,000 nucleotides, our cells become senescent, or simply go through programmed cell death (apoptosis).

What happens when a certain number of cells in our organisms are senescent? Recent epidemiological studies show that the presence of short telomeres is often linked with atherosclerosis, hypertension, cardiovascular disease, metabolic syndrome, Alzheimer’s, infection, diabetes, fibrosis, and especially cancer risk factors. There is most likely a causal relationship between telomere shortening and global mortality.

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