DNA strands have non-encoding ends called telomeres. Telomeres are a non-encoding G-rich repeating sequence of base units that tells the cellular DNA replicative machinery that it’s reached the end of the DNA strand and prevents the ends of different DNA strands from being fused together. In humans and all functional vertebrates, that sequence is TTAGGG.

You can read about the details of nucleic acid synthesis here. One of the DNA strands can not be copied sequentially. Instead, primers are attached and replication happens backwards from that location. The resulting DNA segments are stitched together by another enzyme. This method can not replicate the very end of the DNA strand. Were it not for telomeres, coding DNA would be lost with each replication.

The telomeres perform another function. If it were not for some marker, enzymes that repair double strand DNA breaks would confuse the ends of two different chromosomes for a broken DNA strand and fuse them. Normally, when telomeres are shorted beyond a critical point, replication stops. Occasionally this type of DNA mutation happens.

Telomerase is an enzyme that adds additional base units back on to telomeres restoring their length. Telomerase is not active in normal somatic cells. DNA which codes for telomerase is present in every cell but transcription is prevented by methylation of that section of DNA. However, telomerase is active in germ cells and in proliferating cells such as the bone marrow stem cells that produce red blood cells. Actually this oversimplifies things greatly, the regulation of telomerase is actually quite complex involving other genes and proteins and is not a simple all or nothing proposition.

Initially life involved either self-replicating proteins or single strand RNA. Double strand DNA offered a form of checksum. It offered additional genetic stability that probably gave it a competitive advantage. Initially, DNA was probably in the form of a ring which allowed full sequential copying of both strands. Telomeres evolved allowing limited copying of non-circular strands of DNA. Eventually telomerase evolved providing a method of restoring the length of the telomeres.

The lack telomerase in some cells evolved not to promote the survival of the individual by providing a barrier to cancer, but rather to provide for programmed death and higher mutation rates giving our species an ability to more rapidly adapt to a changing environment. If the individuals lived significantly longer and the mutation rate was lower, genetic adaptation of our species would be slower. The suppression of telomerese in most cells was an additional evolutionary step promoting the survival of the species in a rapidly changing environment.

That our genes would posses sequences that promote the survival of the group over that of the individual is nothing new, we see examples of that in our behavior which is also genetically determined. We have a set of behaviors designed to promote the survival of the individual which we often consider primitive and which corresponds with the label, “The Id”, and we have a collection of behaviors that are geared towards the survival of the group which corresponds with the label, “The Superego”.

DNA which has the highest tendency to propagate successfully survives. Any quality that enhances the likelihood that a given DNA sequence will be propagated to future generations selects for that sequence. By programming the death of an organism, it can increase the survival fitness of the group, and thus itself.

Sharks have telomerase, an enzyme which lengthens telomeres, active in every cell in their body. Their telomeres don’t shorten and sharks do not have a genetically programmed life span the way humans do. Sharks keep growing throughout their entire life. The limit to their lifespan is the fact that they must keep moving in order for water to circulate through their gills so that they get oxygen they need to survive. Sharks rarely get cancer. Sharks also are exceptionally genetically stable, having changed very little in hundreds of millions of years.

In humans, telomerase is active in germ cells so that each new generation begins with a full length set of telomerese. The stem cells in the bone marrow that produce red blood cells has telomerase activity allowing them to reproduce the large number of generations necessary to replace cells that only live on average three days.

If the function of telomeres was to prevent cancer by limiting the number of cellular generations, we would expect to die within about a week of birth from leukemia, both because that protection afforded by telomere shortening is not present and because blood cells reproduce extremely rapidly. Telomerase introduced into human tissue cultures to allow the cell lines to reproduce indefinitely did not cause cancer.

Telomeres do protect against cancer by preventing the ends of DNA strands from being recognized as a double strand DNA break and fused with other DNA strands. It is also possible that the competition between telomerase and telomere shortening during reproduction provides a competition that limits the rate that cells containing telomerase can reproduce as opposed to an absolute limit on generations, and in that way limit potential cancer growth.

Leukemia and other blood cancers are relatively rare. Lung, stomach, co-rectal, prostate, liver, bladder, esophagus, and oral cancers are all more common than leukemia. In addition, in humans, we also find that as we age and the telomeres get shorter, DNA transcription errors increase and mutations and cancer rates increase with them.

If the cancer protectant theory of telomeres were correct, shorter telomeres would have the effect of putting the brakes on sooner, reducing the likelihood that a cell with a defect enabling uncontrolled replication would mutate into one in which the genes for telomerase was expressed and turning into full blown cancer. If not here to protect us from cancer, why then do most of our cells have the genetic machinery for creating telomerase turned off?

Picture this; there are groups of mammals, one group develops a mutation that suppresses the expression of telomerase maybe not entirely but to the point where it’s less efficient than others. This causes the individuals of this group to live a finite lifespan, where members of the other group live indefinitely save for accidents, predation, or starvation. That is to say the other group has no programmed lifespan.

The group with the telomerase suppression also has more mutations, more birth defects. The group adapts to these changes by reproducing at a higher rate enabling the group to maintain it’s population against environmental limits just as the group without the mutation does.

Now, imagine a rapidly changing environment. The group without the mutation live longer and have a slower reproductive rate. A generation takes more years to pass. They have lower mutation rates so adaptive mutations take more generations to occur.

The group with the mutations, new generations come more frequently and adaptive mutations occur more frequently. In a rapidly changing environment, they out compete the more stable group.

This, in a nutshell, is why I believe we have the genetic code that disables telomerase evolved, it provided a competitive advantage to the group, even though it limited the lifespan of the individual.

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