Day 074 - The mitotic clock

Submitted by Sam on 3 August, 2011 - 00:48

Telomeres are repetitive DNA sequences which cap the ends of chromosomes, protecting them from damage and potentially cancerous breakages and fusings. They act as disposable buffers, much as the plastic aglets at the end of shoelaces prevent fraying. Each time a cell divides, the telomores get shorter as DNA sequences are lost from the end. When telomeres reach a certain critical length, the cell is unable to make new copies of itself, and so organs and tissues that depend on continued cell replication begin to senesce. The shortening of telomeres plays a large part in ageing (although not necessarily a causal one), and so advocates of life extension are exploring the possibility of lengthening telomeres in certain cells by searching for ways to selectively activate the enzyme telomerase, which maintains telemore length by the adding newly synthesized DNA code to their ends. If we could induce certain parts of our bodies to express more telomerase, the theory goes, we will be able to live longer, healthier lives, slowing down the decline of ageing.

Every moment we're fighting a losing battle against our telomeric shortening; at conception our telomeres consist of roughly 15,000 DNA base pairs, shrinking to 10,000 at birth when the telomerase gene becomes largely deactivated. Without the maintenance work of the enzyme our telomeres reduce in length at a rate of about 50 base pairs a year. When some telomeres drop below 5,000 base pairs, their cells lose the ability to divide, becoming unable to perform the work they were designed to carry out, and in some cases also releasing chemicals that are harmful to neighbouring cells. Some particularly prominent cell-types that are affected by the replicative shortening of telomeres include the endothelial cells lining blood vessels leading to the heart, and the cells that make the myelin sheath that protects our brain's neurons. Both brain health and heart health are bound to some degree to the fate of cells with a telomeric fuse. The correlation between telomere length and biological ageing has motivated a hope that one day we will be able to prevent and perhaps reverse the effects of replicative senescence by optimally controlling the action of telomerase.

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