How Does Telomerase Work?

Telomeres are located at the very tips of chromosomes and are repeating DNA sequences of six nucleotides - TTAGGG. Telomeres prevent chromosomes from losing base pair sequences near their ends, and they prevent DNA strands from fusing together. The molecular biologist Elizabeth Blackburn (co-discoverer of telomerase) has compared them to the tips of shoelaces that prevent the laces from fraying.

Every time a cell divides the telomeres shorten, and when they reach a critical length the cell can no longer divide and it dies. Telomere length is determined by the loss and addition of base pairs. Cell division causes the loss, and the enzyme telomerase is responsible for the addition.

The telomerase enzyme is made of proteins and RNA subunits which extend the length of chromosomes by adding TTAGGG sequences; the nucleotides are added to the 3' ends of DNA strands. It is a reverse transcriptase enzyme which means that it transcribes its own single-stranded RNA molecule into a single strand of DNA

Cells are dividing all the time, to produce new cells and replace old ones, but our regular somatic cells do not use telomerase, and without the telomeres being renewed the cell eventually dies - cell senescence. Telomerase though is active in our germ cells, stem cells, and in tumour cells. Knowledge of telomerase activity has led to some scientists proposing the idea of creating an "immortal" cell by finding a way of switching on the enzyme in adult cells. And this naturally leads to the far-fetched idea of using telomerase to halt the ageing process completely. Although it may not put an end to ageing, the potential is there to at least slow it down, and/or minimise some of its effects.

The immediate benefits of telemorase activity research may come to cancer studies. It is known that telomerase is much more active in cancer cells than normal cells. It's been implicated in about 90% of tumours.

Cancer cells are immortal; they refuse to grow up, and just keep on dividing - and telomerase is the cause of this in many types of cancer. The enzyme prevents the telomeres from shortening which prolongs the life of the malignant cell.

If a way could be found to "switch off" the enzyme the possibility exists that the cancer could be halted because the telomeres would begin to shorten - and so the malignant cells would eventually die out. No longer would they be immortal. Science is not even at human clinical trials with this idea yet, but the potential for this as a cancer treatment is huge, and has opened up ambitious new areas of research.