2009 Nobel Prize for medicine: Elizabeth Blackburn, Carol Greider, Jack Szostak

as cells age, they stop dividing. Anti-ageing solutions can get them to change their mind, but only temporarily. There comes a time when a cell gives up. This is because the agent that controls cell division is worn out. It is the discovery of this agent—the telomere and the associated enzyme telomerase—that bagged the 2009 Nobel Prize for medicine.

A cell cannot divide if its blueprint—the dna that is contained in the chromosomes – is damaged in anyway.

Since the 1930s, scientists knew that chromosomes were protected. But they were not sure what protected them, and how. Research by three scientists led to the discovery of the protective agent, now known as the telomere.

In the 1980s, Elizabeth Blackburn, biologist from the University of California in San Francisco in usa, and one of the recipients of the Nobel Prize, discovered a small dna sequence-plus-protein unit at the end of the chromosomes. Meanwhile, Jack Szostak, the second biologist to receive the prize, created, from viruses, small chromosome-like pieces called minichromosomes with proteins attached. These he introduced into yeast cells to observe their function but he could not; they degraded every time the cell divided.

Soon, Szostak, who is from the Harvard Medical School in usa, heard about Blackburn’s discovery and thought it wise to collaborate with her. This time the minichromosomes, well-capped by Blackburn’s discovery, were introduced into the yeast cells. Result: the minichromosomes did not degrade.

Delving into its workings, the duo found that the small dna sequence acted as the minichromosome’s guardian, protecting it from damage. This sequence was named the telomere.

Telomeres are denoted by the letter that represents the gene. Though the teomere does not code for proteins, it is not junk either. As Blackburn puts it, telomeres are like the protective cap at the end of shoelaces. Remove the cap and the shoelace unravels.

A few years later, Blackburn and her graduate student, Carol W Greider, now at the Johns Hopkins University and the third recipient, discovered an enzyme in a single-celled organism. Only in the enzyme’s presence did the telomeres not shorten every time the cell divided.

Other researchers confirmed this in people suffering from rare genetic mutation that causes them to produce low amounts of telomerase. The length of their telomeres shortens fast to the extent that they cannot protect the chromosomes from unravelling. This makes the dna unstable which translates into diseases like cancer. One way or another, their immune system gives up too because bone marrow stem cells—the source—stop dividing. Such people do not survive beyond middle age.

Keeping telomerase’s function in mind, researchers are targeting its production to stop harmful cells from dividing. This enzyme is the buzzword in cancer research these days.

But the presence of telomerase does not end all troubles. Just like a tape recorder cannot play the last few seconds of a cassette, the replication of the telomere is such that it does shorten very slightly with every cell division. This is the unavoidable deal of ageing and, finally, cell death, under normal circumstances. But people do not always lead normal lives. They smoke, eat junk food. These factors go a long way to impact the telomerase production which decides their fate eventually.


Telomerase quantified

Blackburn and her colleague studied mothers with chronically ill children where the mother took care of her child by herself. Those under high stress produced telomerase in low amounts and had shorter telomere length.

A study, involving 29,000 people in 52 countries across six continents, found that cardiovascular disease risk factors (smoking, stress, diabetes, abdominal obesity) were related to lower telomerase activity. When compared, non-smokers were much better placed than smokers who showed low amounts of telomerase even at rest. Volunteers were asked to give a speech in front of an audience. The audience had trained subjects who betrayed no reaction throughout. This agitated some and their pulse began to race. These people were the ones that showed low telomerase activity at rest. This indicates the heart’s ability to adapt to situations and how prone it is to disease risks.


In a nutshell

An anti-ageing solution is not where the hard-earned money should be invested. Telomerase maintains the telomere’s length, ensures a long lifespan. So one can invest in telomerase by not smoking, eating junk food and stressing if one wants to give life a chance.